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Cabergoline (brand names Dostinex and others), an ergot derivative, is a potent dopamine receptor agonist on D 2 receptors. Rat studies show cabergoline has a direct inhibitory effect on pituitary lactotroph ( prolactin ) cells. It is frequently used as a first-line agent in the management of prolactinomas due to its higher affinity for D 2 receptor sites, less severe side effects, and more convenient dosing schedule than the older bromocriptine, though in pregnancy bromocripine is often still chosen since there is less data on safety in pregnancy for cabergoline.
Contents
1 Medical uses
1.1 Off-label
1.2 Pregnancy and lactation
2 Contraindications and precautions
3 Side effects
3.1 Valvular heart disease
4 Interactions
5 Pharmacology
5.1 Binding profile
6 Pharmacokinetics
7 Mechanism of action
8 Research
9 History
10 See also
11 References
12 External links
Medical uses
Lactation suppression
hyperprolactinemia
adjunctive therapy of prolactin-producing pituitary gland tumors ( prolactinomas );
monotherapy of Parkinson’s disease in the early phase;
combination therapy, together with levodopa and a decarboxylase inhibitor such as carbidopa, in progressive-phase Parkinson’s disease;
in some countries also: ablactation and dysfunctions associated with hyperprolactinemia ( amenorrhea, oligomenorrhea, anovulation, nonpuerperal mastitis and galactorrhea );
treatment of uterine fibroids.
adjunctive therapy of acromegaly, cabergoline has low efficacy in suppressing growth hormone levels and is highly efficient in suppressing hyperprolactinemia that is present in 20-30% of acromegaly cases; growth hormone and prolactin are similar structurally and have similar effects in many target tissues, therefore targeting prolactin may help symptoms when growth hormone secretion can not be sufficiently controlled by other methods;
Off-label
It has at times been used as an adjunct to SSRI antidepressants as there is some evidence that it counteracts certain side effects of those drugs, such as reduced libido and anorgasmia. It also has been suggested that it has a possible recreational use in reducing or eliminating the male refractory period, thereby allowing men to experience multiple ejaculatory orgasms in rapid succession, and at least two scientific studies support those speculations.
Pregnancy and lactation
Relatively little is known about the effects of this medication during pregnancy and lactation. In some cases the related bromocriptine may be an alternative when pregnancy is expected.
Pregnancy : available preliminary data indicates a somewhat increased rate of congenital abnormalities in patients who became pregnant while treated with cabergoline.
Lactation : In rats cabergoline was found in the maternal milk. Since it is not known if this effect also occurs in humans, breastfeeding is usually not recommended if/when treatment with cabergoline is necessary.
Lactation suppression : In some countries cabergoline (Dostinex) is sometimes used as a lactation suppressant. It is also used in veterinary medicine to treat false pregnancy in dogs.
Contraindications and precautions
Hypersensitivity to ergot derivatives
Pediatric patients (no clinical experience)
Severely impaired liver function or cholestasis
Co-medication with drugs metabolized mainly by CYP P450 such as erythromycin and ketoconazole, because increased plasma levels of cabergoline may result (although cabergoline undergoes minimal CYP450 metabolism).
Cautions: severe cardiovascular disease, Raynaud’s disease, gastroduodenal ulcers, active gastrointestinal bleeding, hypotension.
Side effects
Side effects are mostly dose dependent. Much more severe side effects are reported for treatment of Parkinson’s disease and (off-label treatment) for restless leg syndrome which both typically require very high doses. The side effects are considered mild when used for treatment of hyperprolactinemia and other endocrine disorders or gynecologic indications where the typical dose is one hundredth to one tenth that for Parkinson’s disease.
Cabergoline requires slow dose titration (2–4 weeks for hyperprolactinemia, often much longer for other conditions) to minimise side effects. The extremely long bioavailability of the medication may complicate dosing regimens during titration and require particular precautions.
Cabergoline is considered the best tolerable option for hyperprolactinemia treatment although the newer and less tested quinagolide may offer similarly favourable side effect profile with quicker titration times.
Approximately 200 patients with newly diagnosed Parkinson’s disease participated in a clinical study of cabergoline monotherapy. Seventy-nine (79) percent reported at least one side effect. These side effects were chiefly mild or moderate:
GI tract: Side effects were extremely frequent. Fifty-three percent of patients reported side effects. Very frequent: Nausea (30%), constipation (22%), and dry mouth (10%). Frequent: Gastric irritation (7%), vomiting (5%), and dyspepsia (2%).
Psychiatric disturbances and central nervous system (CNS): Altogether 51 percent of patients were affected. Very frequent: Sleep disturbances ( somnolence 18%, insomnia 11%), vertigo (27%), and depression (13%). Frequent: dyskinesia (4%) and hallucinations (4%).
Cardiovascular: Approximately 30 percent of patients experienced side effects. Most frequent were hypotension (10%), peripheral edema (14%) and non-specific edema (2%). Arrhythmias were encountered in 4.8%, palpitations in 4.3%, and angina pectoris in 1.4%.
In a combination study with 2,000 patients also treated with levodopa, the incidence and severity of side effects was comparable to monotherapy. Encountered side effects required a termination of cabergoline treatment in 15% of patients. Additional side effects were infrequent cases of hematological side effects, and an occasional increase in liver enzymes or serum creatinine without signs or symptoms.
As with other ergot derivatives, pleuritis, exudative pleura disease, pleura fibrosis, lung fibrosis, and pericarditis are seen. These side effects are noted in less than 2% of patients. They require immediate termination of treatment. Clinical improvement and normalization of X-ray findings are normally seen soon after cabergoline withdrawal. It appears that the dose typically used for treatment of hyperprolactinemia is too low to cause this type of side effects.
Valvular heart disease
In two studies published in the New England Journal of Medicine on January 4, 2007, cabergoline was implicated along with pergolide in causing valvular heart disease.
Interactions
No interactions were noted with levodopa or selegiline. The drug should not be combined with other ergot derivatives. Dopamine antagonists such as antipsychotics and metoclopramide counteract some effects of cabergoline. The use of antihypertensive drugs should be intensively monitored because excessive hypotension may result from the combination.
Pharmacology
Although cabergoline is commonly described principally as a dopamine D 2 receptor agonist, it also possesses significant affinity for the D 3, D 4, 5-HT 1A, 5-HT 2A, 5-HT 2B, 5-HT 2C, α 2B – receptors, and moderate/low affinity for the D 1 and 5-HT 7 receptors. Cabergoline functions as an agonist at all of these receptors except for 5-HT 7 and α 2B -, where it acts as an antagonist.
Binding profile
Receptor
Binding Affinity (K i [nM])
Action
5-HT 1A
20.0
Agonist
5-HT 1B
479
Unknown
5-HT 1D
8.71
Unknown
5-HT 2A
6.17
Agonist
5-HT 2B
1.17
Agonist
5-HT 2C
692
Agonist
α 1A adrenergic
288
Unknown
α 1B adrenergic
60.3
Unknown
α 1D adrenergic
166
Unknown
α 2A adrenergic
12
Unknown
α 2B adrenergic
72.4
Antagonist
α 2C adrenergic
22.4
Unknown
β 1 adrenergic
>10,000
Unknown
β 2 adrenergic
>10,000
Unknown
D 1
214
Agonist
D 2S
0.62
Agonist
D 2L
0.95
Agonist
D 3
0.79
Agonist
D 4
56.2
Agonist
D 5
22.4
Unknown
Pharmacokinetics
Following a single oral dose, resorption of cabergoline from the gastrointestinal (GI) tract is highly variable, typically occurring within 0.5 to 4 hours. Ingestion with food does not alter its absorption rate. Human bioavailability has not been determined since the drug is intended for oral use only. In mice and rats the absolute bioavailability has been determined to be 30 and 63 percent, respectively. Cabergoline is rapidly and extensively metabolized in the liver and excreted in bile and to a lesser extent in urine. All metabolites are less active than the parental drug or inactive altogether. The human elimination half-life is estimated to be 63 to 68 hours in patients with Parkinson’s disease and 79 to 115 hours in patients with pituitary tumors. Average elimination half-life is 80 hours.
The therapeutic effect in treatment of hyperprolactinemia will typically persist for at least 4 weeks after cessation of treatment.
Mechanism of action
Cabergoline is a long-acting dopamine D 2 receptor agonist and in vitro rat studies show a direct inhibitory effect on the prolactin secretion in the pituitary’s lactotroph cells. Cabergoline decreased serum prolactin levels in reserpinized rats.
Receptor binding studies indicate a low affinity for dopamine D 1 receptors, α 1 -adrenergic receptors, and α 2 -adrenergic receptors.
Research
Cabergoline was studied in one person with Cushing’s disease, to lower ACTH levels and cause regression of ACTH producing pituitary adenomas.
History
Cabergoline was first synthesized by scientists working for the Italian drug company Farmitalia-Carlo Erba in Milan who were experimenting with semisynthetic derivatives of the ergot alkaloids, and a patent application was filed in 1980.
Farmitalia-Carlo Erba was acquired by Pharmacia in 1993,
Cabergoline was first marketed in The Netherlands as Dostinex in 1992.
See also
Bromocriptine

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Indometacin ( INN ; or USAN indomethacin ) is a nonsteroidal anti-inflammatory drug (NSAID) commonly used as a prescription medication to reduce fever, pain, stiffness, and swelling from inflammation. It works by inhibiting the production of prostaglandins, endogenous signaling molecules known to cause these symptoms. It does this by inhibiting cyclooxygenase, an enzyme that catalyzes the production of prostaglandins.
It is marketed under more than twelve different trade names.
Contents
1 Medical uses
2 Contraindications
3 Adverse effects
4 Toxicity
5 Mechanism of action
6 History
7 Society and culture
7.1 Generic names
8 See also
9 References
10 External links
Medical uses
As an NSAID, indometacin is an analgesic, anti-inflammatory, and antipyretic. Clinical indications for indometacin include:
Joint diseases
rheumatoid arthritis
ankylosing spondylitis
osteoarthritis
gouty arthritis
acute painful shoulder bursitis or tendinitis
Headaches
Trigeminal autonomic cephalgias
Paroxysmal hemicranias
Chronic paroxysmal hemicrania
Episodic paroxysmal hemicrania
Hemicrania continua
Valsalva-induced headaches
Primary cough headache
Primary exertional headache
Primary headache associated with sexual activity (preorgasmic and orgasmic)
Primary stabbing headache (jabs and jolts syndrome)
Hypnic headache
Others
Patent ductus arteriosus
Indometacin has also been used clinically to delay premature labor, reduce amniotic fluid in polyhydramnios, and to close patent ductus arteriosus.
Indometacin is a potent drug with many serious side effects and should not be considered an analgesic for minor aches and pains or fever. The medication is better described as an anti-inflammatory, rather than an analgesic. Indometacin can also affect warfarin and subsequently raise INR.
Contraindications
Concurrent peptic ulcer, or history of ulcer disease
Allergy to indometacin, aspirin, or other NSAIDs
Roux-en-Y gastric bypass and gastric sleeve patients
Patients with nasal polyps reacting with an angioedema to other NSAIDs
Children under 2 years of age (with the exception of neonates with patent ductus arteriosus )
Severe pre-existing renal and liver damage
Caution: pre-existing bone marrow damage (frequent blood cell counts are indicated)
Caution: bleeding tendencies of unknown origin (indometacin inhibits platelet aggregation)
Caution: Parkinson’s disease, epilepsy, psychotic disorders (indometacin may worsen these conditions)
Concurrent with potassium sparing diuretics
Patients who have a patent ductus arteriosus dependent heart defect (such as transposition of the great vessels )
Significant hypertension (high blood pressure)
Concomitant administration of lithium salts (such as lithium carbonate)
Adverse effects
See also: Nonsteroidal anti-inflammatory drug
In general, adverse effects seen with indometacin are similar to all other NSAIDs. For instance, indometacin inhibits both cyclooxygenase-1 and cyclooxygenase-2, which then inhibits the production of prostaglandins in the stomach and intestines responsible for maintaining the mucous lining of the gastrointestinal tract. Indometacin, therefore, like other non-selective COX inhibitors can cause peptic ulcers. These ulcers can result in serious bleeding and/or perforation requiring hospitalization of the patient.
To reduce the possibility of peptic ulcers, indometacin should be prescribed at the lowest dosage needed to achieve a therapeutic effect, usually between 50–200 mg/day. It should always be taken with food. Nearly all patients benefit from an ulcer protective drug (e.g. highly dosed antacids, ranitidine 150 mg at bedtime, or omeprazole 20 mg at bedtime). Other common gastrointestinal complaints, including dyspepsia, heartburn and mild diarrhea are less serious and rarely require discontinuation of indometacin.
Many NSAIDs, but particularly indometacin, cause lithium retention by reducing its excretion by the kidneys. Thus indometacin users have an elevated risk of lithium toxicity. For patients taking lithium (e.g. for treatment of depression or bipolar disorder ), less toxic NSAIDs such as sulindac or aspirin are preferred.
All NSAIDs, including indometacin, also increase plasma renin activity and aldosterone levels, and increase sodium and potassium retention. Vasopressin activity is also enhanced. Together these may lead to:
Edema (swelling due to fluid retention)
Hyperkalemia (high potassium levels)
Hypernatremia (high sodium levels)
Hypertension
Elevations of serum creatinine and more serious renal damage such as acute renal failure, chronic nephritis and nephrotic syndrome, are also possible. These conditions also often begin with edema and hyperkalemia.
Paradoxically yet uncommonly, indometacin can cause headache (10 to 20%), sometimes with vertigo and dizziness, hearing loss, tinnitus, blurred vision (with or without retinal damage). There are unsubstantiated reports of worsening Parkinson’s disease, epilepsy, and psychiatric disorders. Cases of life-threatening shock (including angioedema, sweating, severe hypotension and tachycardia as well as acute bronchospasm ), severe or lethal hepatitis and severe bone marrow damage have all been reported. Skin reactions and photosensitivity are also possible side effects.
The frequency and severity of side effects and the availability of better tolerated alternatives make indometacin today a drug of second choice. Its use in acute gout attacks and in dysmenorrhea is well-established because in these indications the duration of treatment is limited to a few days only, therefore serious side effects are not likely to occur.
People should undergo regular physical examination to detect edema and signs of central nervous side effects. Blood pressure checks will reveal development of hypertension. Periodic serum electrolyte (sodium, potassium, chloride) measurements, complete blood cell counts and assessment of liver enzymes as well as of creatinine (renal function) should be performed. This is particularly important if Indometacin is given together with an ACE inhibitor or with potassium-sparing diuretics, because these combinations can lead to hyperkalemia and/or serious kidney failure. No examinations are necessary if only the topical preparations (spray or gel) are applied.
Rare cases have shown that use of this medication by pregnant women can have an effect on the fetal heart, possibly resulting in fetal death via premature closing of the Ductus arteriosus.
Toxicity
Indometacin has a high acute toxicity both for animals (in rats, 12 mg/kg) and for humans. Exact human data does not exist, but some fatal human cases, particularly in children and adolescents, have been seen.
Generally, overdose in humans causes drowsiness, dizziness, severe headache, mental confusion, paresthesia, numbness of limbs, nausea and vomiting. Severe gastrointestinal bleeding is also possible. Cerebral edema, and cardiac arrest with fatal outcome have been seen in children.
The treatment is symptomatic and largely the same as with diclofenac. However, the possibility of severe GI tract symptoms should be particularly noted.
The risk of overdose after exaggerated local treatment with gel or spray is very limited.
Mechanism of action
Main article: Non-steroidal anti-inflammatory drug
Indometacin, a non-steroidal anti-inflammatory drug (NSAID), has similar mode of action when compared to other drugs in this group. Indometacin is a nonselective inhibitor of cyclooxygenase (COX) 1 and 2, the enzymes that participate in prostaglandin synthesis from arachidonic acid. Prostaglandins are hormone -like molecules normally found in the body, where they have a wide variety of effects, some of which lead to pain, fever, and inflammation. By inhibiting the synthesis of prostaglandins, indometacin can reduce pain, fever, and inflammation.
Besides, indometacin has logarithmic acid dissociation constant pKa of 3 to 4.5. Since the physiologic body pH is well above the pKa range of indometacin, most of the indometacin molecules will be disscociated into ionised form, leaving very little unionised form of indometacin to cross a cell membrane. If the pH gradient across a cell membrane is high, most of the indometacin molecules will be trapped in one side of the membrane with higher pH. This phenomenon is called “ion trapping”. The phenomenon of ion trapping is particularly prominent in the stomach as pH at the stomach mucosa layer is extremely acidic, while the parietal cells are more alkaline. Therefore, indometacin are trapped inside the parietal cells in ionised form, damaging the stomach cells, causing stomach irritation. This stomach irritation can reduce if the stomach acid pH is reduced.
Indometacin’s role in treating certain headaches is unique compared to other NSAIDs. In addition to the class effect of COX inhibition, there is evidence that indometacin has the ability to reduce cerebral blood flow not only through modulation of nitric oxide pathways but also via intracranial precapillary vasoconstriction.
Prostaglandins also cause uterine contractions in pregnant women. Indometacin is an effective tocolytic agent, able to delay premature labor by reducing uterine contractions through inhibition of prostaglandin synthesis in the uterus and possibly through calcium channel blockade.
Indometacin readily crosses the placenta and can reduce fetal urine production to treat polyhydramnios. It does so by reducing renal blood flow and increasing renal vascular resistance, possibly by enhancing the effects of vasopressin on the fetal kidneys.
Other modes of action for indometacin are:
it inhibits motility of polymorphonuclear leukocytes, similar to colchicine
it uncouples oxidative phosphorylation in cartilaginous (and hepatic) mitochondria, like salicylates
History
Indometacin was created in 1963
Society and culture
Generic names
Indometacin is the INN, BAN, and JAN of the drug while indomethacin is the USAN, and former AAN and BAN.
See also
Indometacin farnesil
Indometacin morpholinylamide
Pravadoline
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Clarithromycin, sold under the brand name Biaxin among others, is an antibiotic used to treat various bacterial infections.
Common side effects include nausea, vomiting, headaches, and diarrhea.
Clarithromycin was developed in 1980.
Contents
1 Medical uses
1.1 Spectrum of bacterial susceptibility
2 Contraindications
3 Side effects
3.1 Cardiac
3.2 Liver and kidney
3.3 Central nervous system
3.4 Infection
3.5 Pregnancy and breastfeeding
4 Interactions
4.1 Colchicine
4.2 Statins
4.3 Calcium channel blockers
4.4 Carbamazepine
4.5 HIV medications
5 Mechanism of action
6 Pharmacokinetics
7 Metabolism
8 History
9 Society and culture
9.1 Cost
9.2 Available forms
9.3 Brand names
9.4 Manufacturers
10 References
11 External links
Medical uses
Clarithromycin is primarily used to treat a number of bacterial infections including pneumonia, Helicobacter pylori, and as an alternative to penicillin in strep throat. It is effective against upper and lower respiratory tract infections, skin and soft tissue infections and helicobacter pylori infections associated with duodenal ulcers.
Spectrum of bacterial susceptibility
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (February 2018) ( Learn how and when to remove this template message )
Aerobic Gram-positive bacteria
Staphylococcus aureus
Streptococcus pneumoniae
Streptococcus pyogenes
Aerobic Gram-negative bacteria
Haemophilus parainfluenzae 
Haemophilus influenzae
Moraxella catarrhalis
Helicobacter
Helicobacter pylori
Mycobacteria
Mycobacterium avium complex consisting of:
Mycobacterium avium avium
Mycobacterium intracellulare
Other bacteria
Chlamydia pneumoniae
Mycoplasma pneumoniae
Safety and effectiveness of clarithromycin in treating clinical infections due to the following bacteria have not been established in adequate and well-controlled clinical trials:
Aerobic Gram-positive bacteria
Streptococcus agalactiae
Streptococcus (Groups C, F, G)
Viridans group streptococci
Aerobic Gram-negative bacteria
Bordetella pertussis
Legionella pneumophila
Pasteurella multocida
Anaerobic Gram-positive bacteria
Clostridium perfringens
Peptococcus Niger
Propionibacterium acnes
Anaerobic Gram-negative bacteria
Prevotella melaninogenica (formerly Bacteroides melaninogenicus )
Contraindications
Clarithromycin should not be taken by people who are allergic to other macrolides or inactive ingredients in the tablets, including microcrystalline cellulose, croscarmelose sodium, magnesium stearate, and povidone
Clarithromycin should not be used by people with a history of cholestatic jaundice and/or liver dysfunction associated with prior clarithromycin use.
Clarithromycin should not be used in the setting of hypokalaemia (low blood potassium)
Use of clarithromycin with the following medications: cisapride, pimozide, astemizole, terfenadine, ergotamine, ticagrelor, ranolazine or dihydroergotamine is not recommended.
It should not be used with colchicine in people with kidney or liver impairment.
Concomitant use with cholesterol medications such as lovastatin or simvastatin.
Hypersensitivity to clarithromycin or any component of the product, erythromycin, or any macrolide antibiotics.
QT prolongation or ventricular cardiac arrhythmias, including torsade de pointes.
Side effects
The most common side effects are gastrointestinal: diarrhea (3%), nausea (3%), abdominal pain (3%), and vomiting (6%). It also can cause headaches, insomnia, and abnormal liver function tests. Allergic reactions include rashes and anaphylaxis. Less common side effects (<1%) include extreme irritability, hallucinations (auditory and visual), dizziness/motion sickness, and alteration in senses of smell and taste, including a metallic taste. Dry mouth, panic attacks, and nightmares have also been reported, albeit less frequently. Cardiac In February 2018, the FDA issued a Safety Communication warning with respect to an increased risk for heart problems or death with the use of clarithromycin, and has recommended that alternative antibiotics be considered in those with heart disease. Clarithromycin can lead to a prolonged QT interval. In patients with long QT syndrome, cardiac disease, or patients taking other QT-prolonging medications, this can increase risk for life-threatening arrhythmias. In one trial, the use of short-term clarithromycin treatment was correlated with an increased incidence of deaths classified as sudden cardiac deaths in stable coronary heart disease patients not using statins. Liver and kidney Clarithromycin has been known to cause jaundice, cirrhosis, and kidney problems, including renal failure. Central nervous system Common adverse effects of clarithromycin in the central nervous system include dizziness, headaches. Rarely, it can cause ototoxicity, delirium and mania. Infection A risk of oral candidiasis and vaginal candidiasis, due to the elimination of the yeast's natural bacterial competitors by the antibiotic, has also been noted. Pregnancy and breastfeeding Clarithromycin should not be used in pregnant women except in situations where no alternative therapy is appropriate. Interactions Clarithromycin inhibits a liver enzyme, CYP3A4, involved in the metabolism of many other commonly prescribed drugs. Taking clarithromycin with other medications that are metabolized by CYP3A4 may lead to unexpected increases or decreases in drug levels. A few of the common interactions are listed below. Colchicine Clarithromycin has been observed to have a dangerous interaction with colchicine as the result of inhibition of CYP3A4 metabolism and P-glycoprotein transport. Combining these two drugs may lead to fatal colchicine toxicity, particularly in patients with renal insufficiency. Statins Taking clarithromycin concurrently with certain statins (a class of drugs used to reduce blood serum cholesterol levels) increases the risk of side effects, such as muscle aches and muscle break down ( rhabdomyolysis ). Calcium channel blockers Concurrent therapy with calcium channel blocker may increase risk of low blood pressure, kidney failure, and death, compared to pairing calcium channel blockers with azithromycin, a drug similar to clarithromycin but without CYP3A4 inhibition. Carbamazepine Clarithromycin may double the level of carbamazepine in the body by reducing its clearance, which may lead to toxic symptoms of carbamazepine, such as double vision, loss of voluntary body movement, nausea, as well as hyponatremia. HIV medications Depending on the combination of medications, clarithromycin therapy could be contraindicated, require changing doses of some medications, or be acceptable without dose adjustments. Mechanism of action Clarithromycin prevents bacteria from multiplying by acting as a protein synthesis inhibitor. It binds to 23S rRNA, a component of the 50S subunit of the bacterial ribosome, thus inhibiting the translation of peptides. Pharmacokinetics This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (February 2018) ( Learn how and when to remove this template message ) Unlike erythromycin, clarithromycin is acid-stable, so can be taken orally without having to be protected from gastric acids. It is readily absorbed, and diffuses into most tissues and phagocytes. Due to the high concentration in phagocytes, clarithromycin is actively transported to the site of infection. During active phagocytosis, large concentrations of clarithromycin are released; its concentration in the tissues can be over 10 times higher than in plasma. Highest concentrations are found in liver, lung tissue, and stool. Metabolism Clarithromycin has a fairly rapid first-pass metabolism in the liver. Its major metabolites include an inactive metabolite, N-desmethylclarithromycin, and an active metabolite, 14-( R )-hydroxyclarithromycin. Compared to clarithromycin, 14-( R )-hydroxyclarithromycin is less potent against mycobacterial tuberculosis and the Mycobacterium avium complex. Clarithromycin (20%-40%) and its active metabolite (10%-15%) are excreted in urine. Of all the drugs in its class, clarithromycin has the best bioavailability at 50%, which makes it amenable to oral administration. Its elimination half-life is about 3 to 4 hours with 250 mg administered every 12 h, but increased to 5 to 7 h with 500 mg administered every 8 to 12 h. With any of these dosing regimens, the steady-state concentration of this metabolite is generally attained within 3 to 4 days. History Clarithromycin was invented by researchers at the Japanese drug company Taisho Pharmaceutical in 1980. The product emerged through efforts to develop a version of the antibiotic erythromycin that did not experience acid instability in the digestive tract, causing side effects, such as nausea and stomachache. Taisho filed for patent protection for the drug around 1980 and subsequently introduced a branded version of its drug, called Clarith, to the Japanese market in 1991. In 1985, Taisho partnered with the American company Abbott Laboratories for the international rights, and Abbott also gained FDA approval for Biaxin in October 1991. The drug went generic in Europe in 2004 and in the US in mid-2005. Society and culture Cost Clarithromycin is available as a generic medication. Available forms In the United States, clarithromycin is available as immediate release tablets, extended release tablets, and granules for oral suspension. Brand names Clarithromycin is available under several brand names in many different countries, for example Biaxin, Bioclar, Crixan, Claritron, Clarihexal, Clacid, Claritt, Clacee, Clarac, Clariwin, Claripen, Clarem, Claridar, Cloff, Fromilid, Infex, Kalixocin, Karicin, Klaricid, Klaridex, Klacid, Klaram, Klabax, MegaKlar, Monoclar, Resclar, Rithmo, Truclar, Vikrol and Zeclar. Manufacturers In the UK the drug product is manufactured in generic form by a number of manufacturers including Somex Pharma, Ranbaxy, Aptil and Sandoz.

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Diltiazem ( INN ) ( / d ɪ l ˈ t aɪ ə z ɛ m / ) is a nondihydropyridine (non-DHP) calcium channel blocker used in the treatment of hypertension, angina pectoris, and some types of arrhythmia. It relaxes the smooth muscles in the walls of arteries, which opens (dilates) the arteries, allows blood to flow more easily, and lowers blood pressure. Additionally, it lowers blood pressure by acting on the heart itself to reduce the rate, strength, and conduction speed of each beat.
It is also used off-label as a preventive medication for migraine. It is a Class 3 antianginal drug, and a Class IV antiarrhythmic.
Diltiazem is metabolized by, and acts as an inhibitor of the CYP3A4 enzyme, which can cause it to interact with a variety of other medications.
Contents
1 Mechanism
2 Nontherapeutic effects and toxicities
3 Indications
4 Contraindications and precautions
5 Drug interactions
5.1 Beta-blockers
5.2 Quinidine
6 Potential future indications
7 References
8 External links
Mechanism
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Diltiazem is a potent vasodilator, increasing blood flow and variably decreasing the heart rate via strong depression of A-V node conduction. Its pharmacological activity is somewhat similar to verapamil, another nondihydropyridine (non-DHP) calcium channel blocker. Chemically, it is based upon a 1,4-thiazepine ring, making it a benzothiazepine -type calcium channel blocker.
It is a vasodilator of coronary and peripheral vessels, which reduces peripheral resistance and afterload, though not as potent as the dihydropyridine (DHP) calcium channel blockers. This results in minimal reflexive sympathetic changes.
Diltiazem has negative inotropic, chronotropic, and dromotropic effects. This means diltiazem causes a decrease in heart muscle contractility – how strong the beat is, lowering of heart rate – due to slowing of the sinoatrial node, and a slowing of conduction through the atrioventricular node – increasing the time needed for each beat. Each of these effects results in reduced oxygen consumption by the heart, reducing angina symptoms. These effects also reduce blood pressure by causing less blood to be pumped out.
Nontherapeutic effects and toxicities
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Indications
Diltiazem is indicated for:
Stable angina (exercise-induced) – diltiazem increases coronary blood flow and decreases myocardial oxygen consumption, secondary to decreased peripheral resistance, heart rate, and contractility.
Variant angina – it is effective owing to its direct effects on coronary dilation.
Unstable angina ( preinfarction, crescendo ) – diltiazem may be particularly effective if the underlying mechanism is vasospasm.
Myocardial bridge
For supraventricular tachycardias ( PSVT ), diltiazem appears to be as effective as verapamil in treating re-entrant supraventricular tachycardia.
Atrial fibrillation or atrial flutter is another indication. The initial bolus should be 0.25 mg/kg, intravenous (IV).
Because of its vasodilatory effects, diltiazem is useful for treating hypertension. Calcium channel blockers are well tolerated, and especially effective in treating low- renin hypertension.
Contraindications and precautions
In congestive heart failure, patients with reduced ventricular function may not be able to counteract the inotropic and chronotropic effects of diltiazem, the result being an even higher compromise of function.
With SA node or AV conduction disturbances, the use of diltiazem should be avoided in patients with SA or AV nodal abnormalities, because of its negative chronotropic and dromotropic effects.
Low blood pressure patients, with systolic blood pressures below 90 mm Hg, should not be treated with diltiazem.
Diltiazem may paradoxically increase ventricular rate in patients with Wolff-Parkinson-White syndrome because of accessory conduction pathways.
Diltiazem is relatively contraindicated in the presence of sick sinus syndrome, atrioventricular node conduction disturbances, bradycardia, impaired left ventricle function, peripheral artery occlusive disease, and chronic obstructive pulmonary disease.
Drug interactions
Because of its inhibition of hepatic cytochromes CYP3A4, CYP2C9 and CYP2D6, there are a significant number of drug interactions. Some of the more important interactions are listed below.
Beta-blockers
Intravenous diltiazem should be used with caution with beta-blockers because, while the combination is most potent at reducing heart rate, there are rare instances of dysrhythmia and AV node block.
Quinidine
Quinidine should not be used concurrently with calcium channel blockers because of reduced clearance of both drugs and potential pharmacodynamic effects at the SA and AV nodes.
Potential future indications
Diltiazem is prescribed off-label by doctors in the US for prophylaxis of cluster headaches. Some research on diltiazem and other calcium channel antagonists in the treatment and prophylaxis of migraine is ongoing.
Recent research
Diltiazem is also being used in the treatment of anal fissures. It can be taken orally or applied topically with increased effectiveness.

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Indometacin ( INN ; or USAN indomethacin ) is a nonsteroidal anti-inflammatory drug (NSAID) commonly used as a prescription medication to reduce fever, pain, stiffness, and swelling from inflammation. It works by inhibiting the production of prostaglandins, endogenous signaling molecules known to cause these symptoms. It does this by inhibiting cyclooxygenase, an enzyme that catalyzes the production of prostaglandins.
It is marketed under more than twelve different trade names.
Contents
1 Medical uses
2 Contraindications
3 Adverse effects
4 Toxicity
5 Mechanism of action
6 History
7 Society and culture
7.1 Generic names
8 See also
9 References
10 External links
Medical uses
As an NSAID, indometacin is an analgesic, anti-inflammatory, and antipyretic. Clinical indications for indometacin include:
Joint diseases
rheumatoid arthritis
ankylosing spondylitis
osteoarthritis
gouty arthritis
acute painful shoulder bursitis or tendinitis
Headaches
Trigeminal autonomic cephalgias
Paroxysmal hemicranias
Chronic paroxysmal hemicrania
Episodic paroxysmal hemicrania
Hemicrania continua
Valsalva-induced headaches
Primary cough headache
Primary exertional headache
Primary headache associated with sexual activity (preorgasmic and orgasmic)
Primary stabbing headache (jabs and jolts syndrome)
Hypnic headache
Others
Patent ductus arteriosus
Indometacin has also been used clinically to delay premature labor, reduce amniotic fluid in polyhydramnios, and to close patent ductus arteriosus.
Indometacin is a potent drug with many serious side effects and should not be considered an analgesic for minor aches and pains or fever. The medication is better described as an anti-inflammatory, rather than an analgesic. Indometacin can also affect warfarin and subsequently raise INR.
Contraindications
Concurrent peptic ulcer, or history of ulcer disease
Allergy to indometacin, aspirin, or other NSAIDs
Roux-en-Y gastric bypass and gastric sleeve patients
Patients with nasal polyps reacting with an angioedema to other NSAIDs
Children under 2 years of age (with the exception of neonates with patent ductus arteriosus )
Severe pre-existing renal and liver damage
Caution: pre-existing bone marrow damage (frequent blood cell counts are indicated)
Caution: bleeding tendencies of unknown origin (indometacin inhibits platelet aggregation)
Caution: Parkinson’s disease, epilepsy, psychotic disorders (indometacin may worsen these conditions)
Concurrent with potassium sparing diuretics
Patients who have a patent ductus arteriosus dependent heart defect (such as transposition of the great vessels )
Significant hypertension (high blood pressure)
Concomitant administration of lithium salts (such as lithium carbonate)
Adverse effects
See also: Nonsteroidal anti-inflammatory drug
In general, adverse effects seen with indometacin are similar to all other NSAIDs. For instance, indometacin inhibits both cyclooxygenase-1 and cyclooxygenase-2, which then inhibits the production of prostaglandins in the stomach and intestines responsible for maintaining the mucous lining of the gastrointestinal tract. Indometacin, therefore, like other non-selective COX inhibitors can cause peptic ulcers. These ulcers can result in serious bleeding and/or perforation requiring hospitalization of the patient.
To reduce the possibility of peptic ulcers, indometacin should be prescribed at the lowest dosage needed to achieve a therapeutic effect, usually between 50–200 mg/day. It should always be taken with food. Nearly all patients benefit from an ulcer protective drug (e.g. highly dosed antacids, ranitidine 150 mg at bedtime, or omeprazole 20 mg at bedtime). Other common gastrointestinal complaints, including dyspepsia, heartburn and mild diarrhea are less serious and rarely require discontinuation of indometacin.
Many NSAIDs, but particularly indometacin, cause lithium retention by reducing its excretion by the kidneys. Thus indometacin users have an elevated risk of lithium toxicity. For patients taking lithium (e.g. for treatment of depression or bipolar disorder ), less toxic NSAIDs such as sulindac or aspirin are preferred.
All NSAIDs, including indometacin, also increase plasma renin activity and aldosterone levels, and increase sodium and potassium retention. Vasopressin activity is also enhanced. Together these may lead to:
Edema (swelling due to fluid retention)
Hyperkalemia (high potassium levels)
Hypernatremia (high sodium levels)
Hypertension
Elevations of serum creatinine and more serious renal damage such as acute renal failure, chronic nephritis and nephrotic syndrome, are also possible. These conditions also often begin with edema and hyperkalemia.
Paradoxically yet uncommonly, indometacin can cause headache (10 to 20%), sometimes with vertigo and dizziness, hearing loss, tinnitus, blurred vision (with or without retinal damage). There are unsubstantiated reports of worsening Parkinson’s disease, epilepsy, and psychiatric disorders. Cases of life-threatening shock (including angioedema, sweating, severe hypotension and tachycardia as well as acute bronchospasm ), severe or lethal hepatitis and severe bone marrow damage have all been reported. Skin reactions and photosensitivity are also possible side effects.
The frequency and severity of side effects and the availability of better tolerated alternatives make indometacin today a drug of second choice. Its use in acute gout attacks and in dysmenorrhea is well-established because in these indications the duration of treatment is limited to a few days only, therefore serious side effects are not likely to occur.
People should undergo regular physical examination to detect edema and signs of central nervous side effects. Blood pressure checks will reveal development of hypertension. Periodic serum electrolyte (sodium, potassium, chloride) measurements, complete blood cell counts and assessment of liver enzymes as well as of creatinine (renal function) should be performed. This is particularly important if Indometacin is given together with an ACE inhibitor or with potassium-sparing diuretics, because these combinations can lead to hyperkalemia and/or serious kidney failure. No examinations are necessary if only the topical preparations (spray or gel) are applied.
Rare cases have shown that use of this medication by pregnant women can have an effect on the fetal heart, possibly resulting in fetal death via premature closing of the Ductus arteriosus.
Toxicity
Indometacin has a high acute toxicity both for animals (in rats, 12 mg/kg) and for humans. Exact human data does not exist, but some fatal human cases, particularly in children and adolescents, have been seen.
Generally, overdose in humans causes drowsiness, dizziness, severe headache, mental confusion, paresthesia, numbness of limbs, nausea and vomiting. Severe gastrointestinal bleeding is also possible. Cerebral edema, and cardiac arrest with fatal outcome have been seen in children.
The treatment is symptomatic and largely the same as with diclofenac. However, the possibility of severe GI tract symptoms should be particularly noted.
The risk of overdose after exaggerated local treatment with gel or spray is very limited.
Mechanism of action
Main article: Non-steroidal anti-inflammatory drug
Indometacin, a non-steroidal anti-inflammatory drug (NSAID), has similar mode of action when compared to other drugs in this group. Indometacin is a nonselective inhibitor of cyclooxygenase (COX) 1 and 2, the enzymes that participate in prostaglandin synthesis from arachidonic acid. Prostaglandins are hormone -like molecules normally found in the body, where they have a wide variety of effects, some of which lead to pain, fever, and inflammation. By inhibiting the synthesis of prostaglandins, indometacin can reduce pain, fever, and inflammation.
Besides, indometacin has logarithmic acid dissociation constant pKa of 3 to 4.5. Since the physiologic body pH is well above the pKa range of indometacin, most of the indometacin molecules will be disscociated into ionised form, leaving very little unionised form of indometacin to cross a cell membrane. If the pH gradient across a cell membrane is high, most of the indometacin molecules will be trapped in one side of the membrane with higher pH. This phenomenon is called “ion trapping”. The phenomenon of ion trapping is particularly prominent in the stomach as pH at the stomach mucosa layer is extremely acidic, while the parietal cells are more alkaline. Therefore, indometacin are trapped inside the parietal cells in ionised form, damaging the stomach cells, causing stomach irritation. This stomach irritation can reduce if the stomach acid pH is reduced.
Indometacin’s role in treating certain headaches is unique compared to other NSAIDs. In addition to the class effect of COX inhibition, there is evidence that indometacin has the ability to reduce cerebral blood flow not only through modulation of nitric oxide pathways but also via intracranial precapillary vasoconstriction.
Prostaglandins also cause uterine contractions in pregnant women. Indometacin is an effective tocolytic agent, able to delay premature labor by reducing uterine contractions through inhibition of prostaglandin synthesis in the uterus and possibly through calcium channel blockade.
Indometacin readily crosses the placenta and can reduce fetal urine production to treat polyhydramnios. It does so by reducing renal blood flow and increasing renal vascular resistance, possibly by enhancing the effects of vasopressin on the fetal kidneys.
Other modes of action for indometacin are:
it inhibits motility of polymorphonuclear leukocytes, similar to colchicine
it uncouples oxidative phosphorylation in cartilaginous (and hepatic) mitochondria, like salicylates
History
Indometacin was created in 1963
Society and culture
Generic names
Indometacin is the INN, BAN, and JAN of the drug while indomethacin is the USAN, and former AAN and BAN.
See also
Indometacin farnesil
Indometacin morpholinylamide
Pravadoline
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Atorvastatin, marketed under the trade name Lipitor among others, is a member of the medication class known as statins, which are used primarily as a lipid-lowering agent and for prevention of events associated with cardiovascular disease. Like all statins, atorvastatin works by inhibiting HMG-CoA reductase, an enzyme found in liver tissue that plays a key role in production of cholesterol in the body.
Atorvastatin was first made in August 1985 at Warner-Lambert ‘s Parke-Davis research facility in Ann Arbor, Michigan
Contents
1 Medical uses
1.1 Dyslipidemia
1.2 Cardiovascular disease
1.3 Other uses
2 Administration
2.1 Specific populations
3 Contraindications
4 Adverse effects
4.1 Major
4.2 Common
4.3 Other
4.4 Interactions
5 Mechanism of action
6 Pharmacodynamics
7 Pharmacokinetics
7.1 Absorption
7.2 Distribution
7.3 Metabolism
7.4 Excretion
8 Pharmacogenetics
9 Chemical synthesis
10 History
11 Formulations
12 Generic availability
13 Medication recalls
14 References
15 Further reading
16 External links
Medical uses
The primary uses of atorvastatin is for the treatment of dyslipidemia and the prevention of cardiovascular disease :
Dyslipidemia
Hypercholesterolemia as well as increase HDL levels.
Heterozygous familial hypercholesterolemia in pediatric patients
Homozygous familial hypercholesterolemia
Hypertriglyceridemia ( Fredrickson Type IV )
Primary dysbetalipoproteinemia ( Fredrickson Type III )
Combined hyperlipidemia
Cardiovascular disease
Primary prevention of heart attack, stroke, and need for revascularization procedures in patients who have risk factors such as age, smoking, high blood pressure, low HDL-C, and a family history of early heart disease, but have not yet developed clinically evident coronary artery disease.
Secondary prevention of myocardial infarction, stroke, unstable angina,
Myocardial infarction and stroke prophylaxis in patients with type II diabetes
Other uses
There have been recent studies suggesting that high-dose statin therapy plays a plaque-stabilizing role in people suffering from acute coronary syndrome and thrombotic stroke.
Administration
Atorvastatin may be used in combination with bile acid sequestrants and ezetimibe to increase the reduction in cholesterol levels. However, It is not recommended to combine statin medication treatment with certain other cholesterol-lowering medications, particularly fibrates, because this may increase the risk of myopathy-related adverse effects.
While many statin medications should be administered at bedtime for optimal effect, atorvastatin can be dosed at any time of day, as long as it is continually dosed once daily at the same time.
Specific populations
Geriatric : Plasma concentrations of atorvastatin in healthy elderly subjects are higher than those in young adults, and clinical data suggests a greater degree of LDL-lowering at any dose for patients in the population as compared to young adults.
Pediatric : Pharmacokinetic data is not available for this population.
Gender : Plasma concentrations are generally higher in women than in men, but there is no clinically significant difference in the extent of LDL reduction between men and women.
Renal impairment : Renal disease has no influence on plasma concentrations of atorvastatin and dosing need not be adjusted in these patients.
Hemodialysis : Hemodialysis will not significantly alter medication levels or change clinical effect of atorvastatin.
Hepatic impairment : In patients with chronic alcoholic liver disease, levels of atorvastatin may be significantly increased depending upon the extent of liver disease.
Contraindications
Active liver disease: cholestasis, hepatic encephalopathy, hepatitis, and jaundice
Unexplained elevations in AST or ALT levels
Pregnancy : Atorvastatin may cause fetal harm by affecting serum cholesterol and triglyceride levels, which are essential for fetal development.
Breastfeeding : Small amounts of other statin medications have been found to pass into breast milk, although atorvastatin has not been studied, specifically.
Markedly elevated CPK levels or if a myopathy is suspected or diagnosed after dosing of atorvastatin has begun. Very rarely, atorvastatin may cause rhabdomyolysis,
Adverse effects
Major
Type 2 diabetes mellitus, an uncommon class effect of all statins.
Myopathy with elevation of creatine kinase (CK, aka CPK) As mentioned previously, atorvastatin should be discontinued immediately if this occurs.
Persistent liver enzyme abnormalities occurred in 0.7% of patients who received atorvastatin in clinical trials. It is recommended that hepatic function be assessed with laboratory tests before beginning atorvastatin treatment and repeated as clinically indicated thereafter. If evidence of serious liver injury occurs while a patient is taking atorvastatin, it should be discontinued and not restarted until the etiology of the patient’s liver dysfunction is defined. If no other cause is found, atorvastatin should be discontinued permanently.
Common
The following have been shown to occur in 1–10% of patients taking atorvastatin in clinical trials:
Joint pain
Loose stools
Indigestion
Muscle pain
Nausea
High-dose atorvastatin have also been associated with worsening blood sugar control.
Other
In 2014, the Food and Drug Administration (FDA) reported memory loss, forgetfulness and confusion with all statin products including atorvastatin. The symptoms were not serious, and they were rare and reversible on cessation of treatment with the medication.
Interactions
Interactions with clofibrate, fenofibrate, gemfibrozil, which are fibrates used in accessory therapy in many forms of hypercholesterolemia, usually in combination with statins, increase the risk of myopathy and rhabdomyolysis.
Co-administration of atorvastatin with one of CYP3A4 inhibitors such as itraconazole,
Antacids can rarely decrease the plasma concentrations of statin medications, but do not affect the LDL-C -lowering efficacy.
Niacin also is proved to increase the risk of myopathy or rhabdomyolysis.
Some statins may also alter the concentrations of other medications, such as warfarin or digoxin, leading to alterations in effect or a requirement for clinical monitoring.
Vitamin D supplementation lowers atorvastatin and active metabolite concentrations, yet synergistically reduces LDL and total cholesterol concentrations. Grapefruit juice components are known inhibitors of intestinal CYP3A4.
Co-administration of grapefruit juice with atorvastatin may cause an increase in C max and AUC, which can lead to adverse reactions or overdose toxicity.
A few cases of myopathy have been reported when atorvastatin is given with colchicine.
Mechanism of action
Main article: Statin
As with other statins, atorvastatin is a competitive inhibitor of HMG-CoA reductase. Unlike most others, however, it is a completely synthetic compound. HMG-CoA reductase catalyzes the reduction of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to mevalonate, which is the rate-limiting step in hepatic cholesterol biosynthesis. Inhibition of the enzyme decreases de novo cholesterol synthesis, increasing expression of low-density lipoprotein receptors ( LDL receptors ) on hepatocytes. This increases LDL uptake by the hepatocytes, decreasing the amount of LDL-cholesterol in the blood. Like other statins, atorvastatin also reduces blood levels of triglycerides and slightly increases levels of HDL-cholesterol.
Recent studies have shown that in patients suffering from acute coronary syndrome, high-dose statin treatment may play a plaque-stabilizing role. At high doses, statins have anti-inflammatory effects, incite reduction of the necrotic plaque core, and improve endothelial function, leading to plaque stabilization and, sometimes, plaque regression. However, there is an increased risk of statin-associated adverse effects with such high-dose statin treatment.
Pharmacodynamics
The liver is the primary site of action of atorvastatin, as this is the principal site of both cholesterol synthesis and LDL clearance. It is the dosage of atorvastatin, rather than systemic medication concentration, which correlates with extent of LDL-C reduction.
Pharmacokinetics
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2017) ( Learn how and when to remove this template message )
Absorption
Atorvastatin undergoes rapid absorption when taken orally, with an approximate time to maximum plasma concentration ( T max ) of 1–2 h. The absolute bioavailability of the medication is about 14%, but the systemic availability for HMG-CoA reductase activity is approximately 30%. Atorvastatin undergoes high intestinal clearance and first-pass metabolism, which is the main cause for the low systemic availability. Administration of atorvastatin with food produces a 25% reduction in C max (rate of absorption) and a 9% reduction in AUC (extent of absorption), although food does not affect the plasma LDL-C -lowering efficacy of atorvastatin. Evening dose administration is known to reduce the C max and AUC by 30% each. However, time of administration does not affect the plasma LDL-C-lowering efficacy of atorvastatin.
Distribution
The mean volume of distribution of atorvastatin is approximately 381 L. It is highly protein bound (≥98%), and studies have shown it is likely secreted into human breastmilk.
Metabolism
Atorvastatin metabolism is primarily through cytochrome P450 3A4 hydroxylation to form active ortho- and parahydroxylated metabolites, as well as various beta-oxidation metabolites. The ortho- and parahydroxylated metabolites are responsible for 70% of systemic HMG-CoA reductase activity. The ortho-hydroxy metabolite undergoes further metabolism via glucuronidation. As a substrate for the CYP3A4 isozyme, it has shown susceptibility to inhibitors and inducers of CYP3A4 to produce increased or decreased plasma concentrations, respectively. This interaction was tested in vitro with concurrent administration of erythromycin, a known CYP3A4 isozyme inhibitor, which resulted in increased plasma concentrations of atorvastatin. It is also an inhibitor of cytochrome 3A4.
Excretion
Atorvastatin is primarily eliminated via hepatic biliary excretion, with less than 2% recovered in the urine. Bile elimination follows hepatic and/or extrahepatic metabolism. There does not appear to be any entero-hepatic recirculation. Atorvastatin has an approximate elimination half-life of 14 hours. Noteworthy, the HMG-CoA reductase inhibitory activity appears to have a half-life of 20–30 hours, which is thought to be due to the active metabolites. Atorvastatin is also a substrate of the intestinal P-glycoprotein efflux transporter, which pumps the medication back into the intestinal lumen during medication absorption.
In hepatic insufficiency, plasma concentrations of atorvastatin are significantly affected by concurrent liver disease. Patients with Child-Pugh Stage A liver disease show a four-fold increase in both C max and AUC. People with Child Pugh stage B liver disease show a 16-fold increase in C max and an 11-fold increase in AUC.
Geriatric patients (>65   years old) exhibit altered pharmacokinetics of atorvastatin compared to young adults, with mean AUC and C max values that are 40% and 30% higher, respectively. Additionally, healthy elderly patients show a greater pharmacodynamic response to atorvastatin at any dose; therefore, this population may have lower effective doses.
Pharmacogenetics
Several genetic polymorphisms have been found to be associated with a higher incidence of undesirable side effects of atorvastatin. This phenomenon is suspected to be related to increased plasma levels of pharmacologically active metabolites, such as atorvastatin lactone and p-hydroxyatorvastatin. Atorvastatin and its active metabolites may be monitored in potentially susceptible patients using specific chromatographic techniques.
Chemical synthesis
Atorvastatin synthesis in commercial production (process) chemistry. The key step of establishing this medication’s stereocenters, through initial use of an inexpensive natural product ( chiral pool approach).
Atorvastatin synthesis during discovery chemistry. The key step of establishing stereocenters, using of a chiral ester auxiliary approach.
The first synthesis of atorvastatin at Parke-Davis that occurred during drug discovery was racemic followed by chiral chromatographic separation of the enantiomers. An early enantioselective route to atorvastatin made use of an ester chiral auxiliary to set the stereochemistry of the first of the two alcohol functional groups via a diastereoselective aldol reaction.
Once the compound entered pre-clinical development, process chemistry developed a cost-effective and scalable synthesis.
History
Bruce Roth, who was hired by Warner-Lambert as a chemist in 1982, had synthesized an “experimental compound” codenamed CI 981 – later called atorvastatin.
In 1994 the findings of a Merck-funded study were published in The Lancet concluding the efficacy of statins in lowering cholesterol in 4444 Scandinavian patients proving for the first time not only that a “statin reduced ‘bad’ LDL cholesterol but also that it led to a sharp drop in fatal heart attacks among patients with heart disease.”
In 1996 Warner-Lambert entered into a co-marketing agreement with Pfizer to sell Lipitor, and in 2000 Pfizer acquired Warner-Lambert for $90.2   billion.
Pfizer’s patent on atorvastatin expired in November 2011.
Formulations
Pack and tablet of atorvastatin (Lipitor) 40mg
Atorvastatin calcium tablets are marketed by Pfizer under the trade name Lipitor
Generic availability
Pfizer’s US patent on Lipitor expired on 30 November 2011.
In other countries, atorvastatin calcium is made in tablet form by generic medication makers under various brand names including Stator, Atorvastatin Teva, Litorva, Torid, Atoris, Atorlip, Mactor, Lipvas, Sortis, Torvast, Torvacard, Totalip, and Tulip.
Medication recalls
On 9 November 2012, Indian drugmaker Ranbaxy Laboratories Ltd. voluntarily recalled 10-, 20- and 40-mg doses of its generic version of atorvastatin in the United States.

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Celecoxib, sold under the brand name Celebrex among others, is a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID). It is used to treat the pain and inflammation of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain in adults, painful menstruation, and juvenile rheumatoid arthritis in people two years or older.
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Contents
1 Medical uses
1.1 Mental illness
1.2 Familial adenomatous polyposis
2 Adverse effects
2.1 Allergy
2.2 Heart attack and stroke
2.3 Drug interactions
2.4 Pregnancy
3 Mechanism of action
3.1 Anti-inflammatory
3.2 Anti-cancer
4 Structure-activity relationship
5 History
6 Society and culture
6.1 Fabricated efficacy studies
6.2 Availability
7 Research
7.1 Cancer prevention
7.2 Cancer treatment
8 References
9 External links
Medical uses
Celecoxib is used for osteoarthritis, rheumatoid arthritis, acute pain, musculoskeletal pain, painful menstruation, ankylosing spondylitis, and to reduce the number of colon and rectal polyps in people with familial adenomatous polyposis.
For postoperative pain, it is more or less equal to ibuprofen.
Evidence of effects are not clear as a number of studies done by the manufacturer have not been released for independent analysis.
Mental illness
Tentative evidence supports its use in treating a number of psychiatric disorders, including major depression, bipolar disorder, and schizophrenia.
Familial adenomatous polyposis
It has been used to reduce colon and rectal polyps in people with familial adenomatous polyposis, but it is not known if it decreases rates of cancer,
Adverse effects
Cardiovascular events: NSAIDs are associated with an increased risk of serious (and potentially fatal) adverse cardiovascular thrombotic events, including myocardial infarction and stroke. Risk may be increased with duration of use or pre-existing cardiovascular risk factors or disease. Individual cardiovascular risk profiles should be evaluated prior to prescribing. New-onset hypertension or exacerbation of hypertension may occur (NSAIDs may impair response to thiazide or loop diuretics), and may contribute to cardiovascular events; monitor blood pressure and use with caution in patients with hypertension. May cause sodium and fluid retention, use with caution in patients with edema or heart failure. Long-term cardiovascular risk in children has not been evaluated. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of cardiovascular events; alternative therapies should be considered for patients at high risk.
Gastrointestinal events: NSAIDs may increase risk of serious gastrointestinal (GI) ulceration, bleeding, and perforation (may be fatal). These events may occur at any time during therapy and without warning. Use caution with a history of GI disease (bleeding or ulcers), concurrent therapy with aspirin, anticoagulants and/or corticosteroids, smoking, use of alcohol, the elderly or debilitated patients. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of GI adverse events; alternate therapies should be considered for patients at high risk. When used concomitantly with ≤325 mg of aspirin, a substantial increase in the risk of gastrointestinal complications (e.g., ulcer) occurs; concomitant gastroprotective therapy (e.g., proton pump inhibitors) is recommended.
Hematologic effects: Anemia may occur; monitor hemoglobin or hematocrit in people on long-term treatment. Celecoxib does not usually affect prothrombin time, partial thromboplastin time or platelet counts; it does not inhibit platelet aggregation at approved doses.
People with prior history of ulcer disease or GI bleeding require special precaution. Moderate to severe liver impairment or GI toxicity can occur with or without warning symptoms in people treated with NSAIDs.
Allergy
Celecoxib contains a sulfonamide moiety and may cause allergic reactions in those allergic to other sulfonamide-containing drugs. This is in addition to the contraindication in people with severe allergies to other NSAIDs. However, it has a low (reportedly 4%) chance of inducing cutaneous reactions among persons who have a history of such reactions to aspirin or nonselective NSAIDs. NSAIDs may cause serious skin adverse events, including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis; events may occur without warning and in patients without prior known sulfa allergy. Use should be discontinued at first sign of rash (or any other hypersensitivity).
Heart attack and stroke
The coxibs (which includes celecoxib) increase the risk of major cardiovascular problems by about 37% over placebo, according to a 2013 meta-analysis of hundreds of trials.
The COX-2 inhibitor rofecoxib (Vioxx) was removed from the market in 2004 due to its risk. Like all NSAIDs on the US market, celecoxib carries an FDA-mandated “black box warning” for cardiovascular and gastrointestinal risk. In February 2007, the American Heart Association warned that with respect to “patients with a prior history of or at high risk for cardiovascular disease… use of COX-2 inhibitors for pain relief should be limited to patients for whom there are no appropriate alternatives, and then, only in the lowest dose and for the shortest duration necessary.”
In 2005, a study published in the Annals of Internal Medicine found that cardiovascular effects of COX-2 inhibitors differ, depending on the drug.
In 2016, a randomized trial involving more than 24,000 participants provided strong evidence that treatment with celecoxib is not more likely to result in poor cardiovascular outcomes than treatment with naproxen or ibuprofen.
Drug interactions
Celecoxib is predominantly metabolized by cytochrome P450 2C9. Caution must be exercised with concomitant use of 2C9 inhibitors, such as fluconazole, which can greatly elevate celecoxib serum levels.
Pregnancy
In the US FDA’s pregnancy categories, the drug is category C prior to 30 weeks gestation, and category D starting at 30 weeks gestation.
Mechanism of action
Anti-inflammatory
A highly selective reversible inhibitor of the COX-2 isoform of cyclooxygenase, celecoxib inhibits the transformation of arachidonic acid to prostaglandin precursors. Therefore, it has antipyretic, analgesic and anti-inflammatory properties.
Anti-cancer
For its use in reducing colon polyps, celecoxib affects genes and pathways involved in inflammation and malignant transformation in tumors, but not normal tissues.
Celecoxib binds to Cadherin-11 (which may explain the reduction in cancer progression).
Structure-activity relationship
The Searle research group found the two appropriately substituted aromatic rings must reside on adjacent positions about the central ring for adequate COX-2 inhibition. Various modifications can be made to the 1,5-diarylpyrazole moiety to deduce the structure-activity relationship of celecoxib.
Celecoxib is compound 22; the 4-sulfamoylphenyl on the 1-pyrazol substituent is required for COX-2 inhibition and the 4-methyl on the 5-pyrazol system has low steric hindrance to maximize potency, while the 3-trifluoromethyl group provides superior selectivity and potency. Thus, it is reasonable to expect COX-2-selective inhibitors to be more bulky than nonselective NSAIDs.
History
See also: Discovery and development of cyclooxygenase 2 inhibitors
Celecoxib and other COX-2 selective inhibitors, valdecoxib, parecoxib, and mavacoxib, were discovered by a team at the Searle division of Monsanto led by John Talley.
Two lawsuits arose over discovery of celecoxib. Daniel L. Simmons of Brigham Young University discovered the COX-2 enzyme in 1988,
According to the National Academy of Sciences, Philip Needleman, who was vice president of Monsanto in 1989 and president of Searle in 1993 In University of Rochester v. G.D. Searle & Co., 358 F.3d 916 (Fed. Cir. 2004), the University of Rochester claimed that United States Pat. No. 6,048,850 (which claimed a method of inhibiting COX-2 in humans using a compound, without actually disclosing what that compound might be) covered drugs such as celecoxib. The court ruled in favor of Searle, holding in essence that the University had claimed a method requiring, yet provided no written description of, a compound that could inhibit COX-2 and therefore the patent was invalid.
After the withdrawal of rofecoxib from the market in September 2004, celecoxib enjoyed a robust increase in sales. However, the results of the APC trial in December of that year raised concerns that Celebrex might carry risks similar to those of rofecoxib, and Pfizer announced a moratorium on direct-to-consumer advertising of Celebrex soon afterwards. After a significant drop, sales of Celebrex have recovered, and reached $2 billion in 2006.
Pfizer resumed advertising Celebrex in magazines in 2006,
In late 2007, Pfizer released another US television ad for Celebrex, which also discussed celecoxib’s adverse effects in comparison with those of other anti-inflammatory drugs.
Society and culture
Fabricated efficacy studies
Pfizer and its partner, Pharmacia presented findings from their study that Celebrex was “better in protecting the stomach from serious complications than other drugs.”
On March 11, 2009, Scott S. Reuben, former chief of acute pain at Baystate Medical Center, Springfield, Massachusetts, revealed that the data for 21 studies he had authored for the efficacy of the drug (along with others such as Vioxx ) had been fabricated. The analgesic effects of the drugs had been exaggerated. Reuben was also a former paid spokesperson for Pfizer. Although from 2002 to 2007 Pfizer underwrote much of Dr. Reuben’s research and “many of his trials found that Celebrex and Lyrica, Pfizer drugs, were effective against postoperative pain,” Pfizer was not aware of the fraudulent data.
Availability
Pfizer markets celecoxib under the brand name Celebrex, and it is available as oral capsules containing 50, 100, 200 or 400 mg of celecoxib.
It is legally available in many jurisdictions as a generic under several brand names.
Research
Cancer prevention
The role celecoxib might have in reducing the rates of certain cancers has been the subject of many studies. However, no current medical recommendation exists to use this drug for cancer reduction.
The use of celecoxib to reduce the risk of colorectal cancer has been investigated, but neither celecoxib nor any other drug is indicated for this use. has demonstrated cardioprotective effects and is significantly cheaper, but no head-to-head clinical trials have compared the two drugs.
Cancer treatment
Different from cancer prevention, cancer treatment is focused on the therapy of tumors that have already formed and have established themselves inside the patient. Many studies are going on to determine whether celecoxib might be useful for this latter condition.
Certainly, the inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of celecoxib. However, whether inhibition of COX-2 also plays a dominant role in this drug’s anticancer effects is unclear. For example, a recent study with malignant tumor cells showed celecoxib could inhibit the growth of these cells in vitro, but COX-2 played no role in this outcome; even more strikingly, the anticancer effects of celecoxib were also obtained with the use of cancer cell types that do not even contain COX-2.
Additional support for the idea that other targets besides COX-2 are important for celecoxib’s anticancer effects has come from studies with chemically modified versions of celecoxib. Several dozen analogs of celecoxib were generated with small alterations in their chemical structures.

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Common side effects include movement problems, sleepiness, dry mouth, low blood pressure upon standing, and increased weight.
Chlorpromazine was discovered in 1950 and was the first antipsychotic.
Contents
1 Medical uses
1.1 Other
2 Adverse effects
2.1 Contraindications
2.2 Interactions
2.3 Tolerance and withdrawal
3 Pharmacology
3.1 Pharmacokinetics
3.2 Pharmacodynamics
3.3 Peripheral effects
4 History
5 Brand names
6 Veterinary use
7 Research
7.1 Amebocidal ability
8 References
9 External links
Medical uses
Chlorpromazine is classified as a low-potency typical antipsychotic and in the past was used in the treatment of both acute and chronic psychoses, including schizophrenia and the manic phase of bipolar disorder, as well as amphetamine-induced psychosis. Low-potency antipsychotics have more anticholinergic side effects, such as dry mouth, sedation, and constipation, and lower rates of extrapyramidal side effects, while high-potency antipsychotics (such as haloperidol ) have the reverse profile.
In a 2013 comparison of 15 antipsychotics in schizophrenia, chlorpromazine demonstrated mild-standard effectiveness. It was 13% more effective than lurasidone and iloperidone, approximately as effective as ziprasidone and asenapine, and 12-16% less effective than haloperidol, quetiapine, and aripiprazole.
Chlorpromazine has also been used in porphyria and as part of tetanus treatment. It still is recommended for short-term management of severe anxiety and psychotic aggression. Resistant and severe hiccups, severe nausea / emesis, and preanesthetic conditioning are other uses.
Other
Chlorpromazine is occasionally used off-label for treatment of severe migraine.
In Germany, chlorpromazine still carries label indications for insomnia, severe pruritus, and preanesthesia.
Comparison of chlorpromazine to placebo
Measured outcome
Findings in words
Findings in numbers
Quality of evidence
Global effects
Not any improvement (9 weeks – 6 months)
30% less risk of having no improvement in mental state, behaviour and functioning
RR 0.7 CI 0.6 to 0.9
Very low (estimate of effect uncertain)
Relapse (6 months – 2 years)
35% less risk of relapse
RR 0.7 CI 0.5 to 0.9
Adverse effects
See also: List of adverse effects for chlorpromazine
There appears to be a dose-dependent risk for seizures with chlorpromazine treatment.
Chlorpromazine may deposit in ocular tissues when taken in high dosages for long periods of time.
Comparison of chlorpromazine to placebo
Measured outcome
Findings in words
Findings in numbers
Quality of evidence
Adverse effects
Weight gain
5 times more likely to have considerable weight gain, around 40% with chlorpromazine gaining weight
RR 4.9 CI 2.3 to 10.4
Very low (estimate of effect uncertain)
Sedation
3 times more likely to cause sedation, around 30% with chlorpromazine
RR 2.8 CI 2.3 to 3.5
Acute movement disorder
3.5 times more likely to cause easily reversible but unpleasant severe stiffening of muscles, around 6% with chlorpromazine
RR 3.5 CI 1.5 to 8.0
Parkinsonism
2 times more likely to cause parkinsonism (symptoms such as tremor, hesitancy of movement, decreased facial expression), around 17% with chlorpromazine
RR 2.1 CI 1.6 to 2.8
Decreased blood pressure with dizziness
3 times more likely to cause decreased blood pressure and dizziness, around 15% with chlorpromazine
RR 2.4 CI 1.7 to 3.3
Contraindications
Absolute contraindications include:
Circulatory
CNS depression
Coma
Drug intoxication
Bone marrow suppression
Phaeochromocytoma
Hepatic failure
Active liver disease
Previous hypersensitivity (including jaundice, agranulocytosis, etc.) to phenothiazines, especially chlorpromazine, or any of the excipients in the formulation being used.
Relative contraindications include:
Epilepsy
Parkinson’s disease
Myasthenia gravis
Hypoparathyroidism
Prostatic hypertrophy
Very rarely, elongation of the QT interval may occur, increasing the risk of potentially fatal arrhythmias.
Interactions
Consuming food prior to taking chlorpromazine orally limits its absorption, likewise cotreatment with benztropine can also reduce chlorpromazine absorption.
It is also a moderate inhibitor of CYP2D6 and also a substrate for CYP2D6 and hence can inhibit its own metabolism.
Chlorpromazine may also interact with epinephrine (adrenaline) to produce a paradoxical fall in blood pressure.
Other drugs that prolong the QT interval such as quinidine, verapamil, amiodarone, sotalol and methadone may also interact with chlorpromazine to produce additive QT interval prolongation.
Tolerance and withdrawal
The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotic treatment to avoid acute withdrawal syndrome or rapid relapse.
A failure to notice withdrawal symptoms may be due to the relatively long half life of the drug resulting in the extremely slow excretion from the body. However, there are reports of muscular discomfort, exaggeration of psychotic symptoms and movement disorders, and difficulty sleeping when the antipsychotic drug is suddenly withdrawn, but after years of normal doses these effects are not normally seen.
Pharmacology
Pharmacokinetics
Pharmacokinetic parameters of chlorpromazine
Bioavailability
t max
C SS
Protein bound
V d
t 1/2
Details of metabolism
Excretion
Notes
10–80%
1–4 hours (Oral); 6–24 hours (IM)
100–300 ng/mL
90–99%
10–35 L/kg (mean: 22 L/kg)
30±7 hours
CYP2D6, CYP1A2 —mediated into over 10 major metabolites.
Urine (43–65% after 24 hours)
Its high degree of lipophilicity (fat solubility) allows it to be detected in the urine for up to 18 months.
Three common metabolites of chlorpromazine
Pharmacodynamics
Chlorpromazine is a very effective antagonist of D2 dopamine receptors and similar receptors, such as D3 and D5. Unlike most other drugs of this genre, it also has a high affinity for D1 receptors. Blocking these receptors causes diminished neurotransmitter binding in the forebrain, resulting in many different effects. Dopamine, unable to bind with a receptor, causes a feedback loop that causes dopaminergic neurons to release more dopamine. Therefore, upon first taking the drug, patients will experience an increase in dopaminergic neural activity. Eventually, dopamine production of the neurons will drop substantially and dopamine will be removed from the synaptic cleft. At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect.
Chlorpromazine acts as an antagonist (blocking agent) on different postsynaptic and presynaptic receptors:
Dopamine receptors (subtypes D 1, D 2, D 3 and D 4 ), which account for its different antipsychotic properties on productive and unproductive symptoms, in the mesolimbic dopamine system accounts for the antipsychotic effect whereas the blockade in the nigrostriatal system produces the extrapyramidal effects
Serotonin receptors (5-HT 1 and 5-HT 2 ), with anxiolytic, and antiaggressive properties as well as an attenuation of extrapyramidal side effects, but also leading to weight gain and ejaculation difficulties.
Histamine receptors ( H 1 receptors, accounting for sedation, antiemetic effect, vertigo, and weight gain)
α 1 – and α 2 -adrenergic receptors (accounting for sympatholytic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism—controversial. Also associated with weight gain as a result of blockage of the adrenergic alpha 1 receptor)
M 1 and M 2 muscarinic acetylcholine receptors (causing anticholinergic symptoms such as dry mouth, blurred vision, constipation, difficulty or inability to urinate, sinus tachycardia, electrocardiographic changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side effects).
The presumed effectiveness of the antipsychotic drugs relied on their ability to block dopamine receptors. This assumption arose from the dopamine hypothesis that maintains that both schizophrenia and bipolar disorder are a result of excessive dopamine activity. Furthermore, psychomotor stimulants like cocaine that increase dopamine levels can cause psychotic symptoms if taken in excess.
Chlorpromazine and other typical antipsychotics are primarily blockers of D2 receptors. In fact an almost perfect correlation exists between the therapeutic dose of a typical antipsychotic and the drug’s affinity for the D2 receptor. Therefore, a larger dose is required if the drug’s affinity for the D2 receptor is relatively weak. A correlation exists between average clinical potency and affinity of the antipsychotics for dopamine receptors.
Chlorpromazine tends to have greater effect at serotonin receptors than at D2 receptors, which is notably the opposite effect of the other typical antipsychotics. Therefore, chlorpromazine with respect to its effects on dopamine and serotonin receptors is more similar to the atypical antipsychotics than to the typical antipsychotics.
Chlorpromazine and other antipsychotics with sedative properties such as promazine and thioridazine are among the most potent agents at α-adrenergic receptors. Furthermore, they are also among the most potent antipsychotics at histamine H1 receptors. This finding is in agreement with the pharmaceutical development of chlorpromazine and other antipsychotics as anti-histamine agents. Furthermore, the brain has a higher density of histamine H1 receptors than any body organ examined which may account for why chlorpromazine and other phenothiazine antipsychotics are as potent at these sites as the most potent classical antihistamines.
In addition to influencing the neurotransmitters dopamine, serotonin, epinephrine, norepinephrine, and acetylcholine it has been reported that antipsychotic drugs could achieve glutamanergic effects. This mechanism involves direct effects on antipsychotic drugs on glutamate receptors. By using the technique of functional neurochemical assay chlorpromazine and phenothiazine derivatives have been shown to have inhibitory effects on NMDA receptors that appeared to be mediated by action at the Zn site. It was found that there is an increase of NMDA activity at low concentrations and suppression at high concentrations of the drug. No significant difference in glutamate and glycine activity from the effects of chlorpromazine were reported. Further work will be necessary to determine if the influence in NMDA receptors by antipsychotic drugs contributes to their effectiveness.
Chlorpromazine does also act as FIASMA (functional inhibitor of acid sphingomyelinase ).
Peripheral effects
Chlorpromazine is an antagonist to H 1 receptors (provoking antiallergic effects), H 2 receptors (reduction of forming of gastric juice), M 1 and M 2 receptors (dry mouth, reduction in forming of gastric juice) and some 5-HT receptors (different anti-allergic/gastrointestinal actions).
Because it acts on so many receptors, chlorpromazine is often referred to as a ” dirty drug “.
History
Advertisement for Thorazine (chlorpromazine) from the early 1960s
In 1933, the French pharmaceutical company Laboratoires Rhône-Poulenc began to search for new anti-histamines. In 1947, it synthesized promethazine, a phenothiazine derivative, which was found to have more pronounced sedative and antihistaminic effects than earlier drugs.
Following on, Laborit considered whether chlorpromazine may have a role in managing patients with severe burns, Raynaud’s phenomenon, or psychiatric disorders. At the Villejuif Mental Hospital in November 1951, he and Montassut administered an intravenous dose to psychiatrist Cornelia Quarti who was acting as a volunteer. Quarti noted the indifference, but fainted upon getting up to go to the toilet, and so further testing was discontinued ( orthostatic hypotension is a possible side effect of chlorpromazine). Despite this, Laborit continued to push for testing in psychiatric patients during early 1952. Psychiatrists were reluctant initially, but on January 19, 1952, it was administered (alongside pethidine, pentothal and ECT) to Jacques Lh. a 24-year-old manic patient, who responded dramatically, and was discharged after three weeks having received 855 mg of the drug in total.
Pierre Deniker had heard about Laborit’s work from his brother-in-law, who was a surgeon, and ordered chlorpromazine for a clinical trial at the Sainte-Anne Hospital Center in Paris where he was Men’s Service Chief.
Deniker then visited America, where the publication of their work alerted the American psychiatric community that the new treatment might represent a real breakthrough. Heinz Lehmann of the Verdun Protestant Hospital in Montreal trialled it in 70 patients and also noted its striking effects, with patients’ symptoms resolving after many years of unrelenting psychosis.
Rhône-Poulenc licensed chlorpromazine to Smith Kline & French (today’s GlaxoSmithKline ) in 1953. In 1955 it was approved in the United States for the treatment of emesis (vomiting). The effect of this drug in emptying psychiatric hospitals has been compared to that of penicillin and infectious diseases.
Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy,
Brand names
Brand names include Thorazine, Largactil, Hibernal, and Megaphen (sold by Bayer in West-Germany since July 1953 ).
Veterinary use
The veterinary use of chlorpromazine has generally been superseded by use of acepromazine.
Chlorpromazine may be used as an antiemetic in dogs and cats, or, less often, as sedative prior to anesthesia.
It is commonly used to decrease nausea in animals that are too young for other common anti-emetics.
The use of chlorpromazine in food-producing animals is not permitted in the EU, as a maximum residue limit could not be determined following assessment by the European Medicines Agency.
Research
Amebocidal ability
Chlorpromazine has tentative benefit in animals infected with Naegleria fowleri.

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Budesonide ( BUD ), sold under the brand name Pulmicort among others, is a medication of the corticosteroid type.
Common side effects with the inhaled form include respiratory infections, cough, and headaches.
Budesonide was initially patented in 1973.
Contents
1 Medical uses
1.1 Asthma
1.2 Inflammatory bowel disease
1.3 Allergic rhinitis
2 Side effects
3 Contraindications
4 Interactions
5 Pharmacology
6 Pharmacokinetics
7 Chemistry
7.1 Stereoisomerism
8 Society and culture
8.1 Brand names
9 See also
10 References
11 External links
Medical uses
Asthma
Budesonide is nebulized for maintenance and prophylactic treatment of asthma including patients who require oral corticosteroids and those who may benefit from a systemic dose reduction.
Inflammatory bowel disease
Formulations of delayed-release Budesonide are an effective treatment for mild-to-moderately active Crohn’s disease involving the ileum and/or ascending colon.
Budesonide assists in the induction of remission in people with active ulcerative colitis.
Budesonide is highly effective and recommended as the drug of choice in microscopic colitis, for induction and maintenance of remission, and for both the lymphocytic colitis and collagenous colitis forms.
Allergic rhinitis
Nasal spray budesonide is a treatment for allergic rhinitis.
Side effects
Budesonide may cause:
Nose irritation or burning
Bleeding or sores in the nose
Lightheadedness
Upset stomach
Cough
Hoarseness
Dry mouth
Rash
Sore throat
Bad taste in mouth
Change in mucus
Blurred vision
In addition, the following symptoms should be reported immediately:
Difficulty breathing or swelling of the face
White patches in the throat, mouth, or nose
Irregular menstrual periods
Severe acne
On rare occasions, behavioral changes (mostly affecting children)
Contraindications
Budesonide is contraindicated as a primary treatment of status asthmaticus or other acute episode of asthma where intensive measures are required.
Interactions
Those taking tablets or capsules orally should avoid grapefruit juice and echinacea.
Grapefruit juice may double bioavailability of oral budesonide.
Echinacea diminishes bioavailability.
Also, high fat meals delay absorption but do not impede absorption.
Pharmacology
Budesonide is an agonist of glucocorticoid receptors. Among its effects are:
Controls the rate of protein synthesis.
Depresses the migration of polymorphonuclear leukocytes and fibroblasts.
Reverses capillary permeability and lysosomal stabilization at the cellular level to prevent or control inflammation.
Has a potent glucocorticoid activity and weak mineralocorticoid activity.
Pharmacokinetics
Onset of action: Nebulization: 2–8 days; Inhalation: 24 hours
Peak effect: Nebulization: 4–6 weeks; Inhalation: 1–2 weeks
Distribution: 2.2-3.9 L/kg
Protein binding: 85% to 90%
Metabolism: Hepatic via CYP3A4 to two metabolites: 16 alpha-hydroxyprednisolone and 6 beta-hydroxybudesonide; minor activity
Bioavailability: Limited by high first-pass effect; Capsule: 9% to 21%; Nebulization: 6%; Inhalation: 6% to 13%
Half-life elimination: 2-3.6 hours
Time to peak: Capsule: 0.5–10 hours (variable in Crohn’s disease); Nebulization: 10–30 minutes; Inhalation: 1–2 hours; Tablet: 7.4-19.2 hours
Excretion: Urine (60%) and feces as metabolites.
Chemistry
See also: List of corticosteroids and List of corticosteroid cyclic ketals
Budesonide, also known as 11β,21-dihydroxy-16α,17α-(butylidenebis(oxy))pregna-1,4-diene-3,20-dione, is a synthetic pregnane steroid and non- halogenated cyclic ketal corticosteroid.
Stereoisomerism
Budesonide (2 stereoisomers)
(22 R )-configuration
(22 S )-configuration
Society and culture
Brand names
Inhaler for a powder based in budesonide and formoterol
Aeronide (TH); Aquacort (DE); B Cort (CO); Bronex (PH); Budair (MY); Budecort DP (MY); Budenofalk (DE, GB, HK, KP, PH, SG); Budeson (AR); Budeson Aqua (AR); BudeSpray (TH); Budiair (KP); Budicort Respules (IL); Budinide (KSA); Bunase (TH); Clebudan (CN); Cycortide (HK); Denecort (PH); Duasma (TW); Eltair (MY); Entocort (AR, AT, BE, BR, CH, CZ, DK, FI, FR, GB, HK, IE, IL, IT, KP, NL, NO, PL, PT, SE, TR); Giona Easyhaler (MY, SG, TH); Inflammide (PE); Miflonid (CZ); Miflonide (BE, DE, IL, IT, NZ, PT); Neumocort (PY); Novopulmon (DE, FR); Pulmicon Susp for Nebulizer (KP); Pulmicort (AT, BE, BG, BR, CH, CL, CN, CO, CR, CZ, DE, DK, DO, EE, FI, FR, GB, GR, GT, HN, ID, IN, NI, NL, NO, PA, PK, PL, PT, RU, SE, SV, TR, TW, UY, VE, ZA); Pulmicort Nasal Turbohaler (CL, KE, MU, NG); Pulmicort Turbuhaler (KE, MU, NG); Rafton (FR); Rhinocort (AU); Rhinocort Aqua (HK); Rhinoside (GR); Symbicort (FR, US, ZA) Uceris (US)
See also
Azelastine
Fluticasone propionate

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