Erythrityl Tetranitrate

Indication	For the prevention of angina.
Pharmacodynamics	Erythrityl Tetranitrate is a vasodilator with general properties similar to nitroglycerin.
Mechanism of action	Similar to other nitrites and organic nitrates, erythrityl tetranitrate is converted to an active intermediate compound which activates the enzyme guanylate cyclase. This stimulates the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP) which then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Symptoms of overdose include increased intracranial pressure, with any or all of persistent throbbing headache, confusion, and moderate fever; Vertigo; Palpitations; Visual disturbances; Nausea and vomiting (possibly with colic and even bloody diarrhea); Syncope (especially in the upright posture); Air hunger and dyspnea, later followed by reduced ventilatory effort; Diaphoresis, with the skin either flushed or cold and clammy; Heart block and bradycardia; Paralysis; Coma; Seizures; Death.

 Brand Names

Cardilate
Cardiloid
Cardivell
Cardiwell
Tetranitrin
Tetranitrol

  
Interactions

Drug Interactions	Drug Interaction Dihydroergotamine Possible antagonism of action Ergotamine Possible antagonism of action Methysergide Possible antagonism of action
Food Interactions	Avoid alcohol. Take on empty stomach: 1 hour before or 2 hours after meals.

Citation
Reference

Pharmacology Of Ergonovine

Indication	Used to treat postpartum haemorrhage and postabortion haemorrhage in patients with uterine atony.
Pharmacodynamics	Ergonovine belongs to the group of medicines known as ergot alkaloids. These medicines are usually given to stop excessive bleeding that sometimes occurs after abortion or a baby is delivered. They work by causing the muscle of the uterus to contract.
Mechanism of action	Ergonovine directly stimulates the uterine muscle to increase force and frequency of contractions. With usual doses, these contractions precede periods of relaxation; with larger doses, basal uterine tone is elevated and these relaxation periods will be decreased. Contraction of the uterine wall around bleeding vessels at the placental site produces hemostasis. Ergonovine also induces cervical contractions. The sensitivity of the uterus to the oxytocic effect is much greater toward the end of pregnancy. The oxytocic actions of ergonovine are greater than its vascular effects. Ergonovine, like other ergot alkaloids, produces arterial vasoconstriction by stimulation of alpha-adrenergic and serotonin receptors and inhibition of endothelial-derived relaxation factor release. It is a less potent vasoconstrictor than ergotamine. As a diagnostic aid (coronary vasospasm), ergonovine causes vasoconstriction of coronary arteries.
Absorption	Absorption is rapid and complete after oral or intramuscular administration.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Hepatic.
Route of elimination	Thought to be eliminated by non-renal mechanisms (i.e. hepatic metabolism, excretion in feces)
Half life	t1/2 α=10 minutes; t1/2 β=2 hours
Clearance	Not Available
Toxicity	The principal symptoms of overdose are convulsions and gangrene. Other symptoms include bradycardia, confusion, diarrhoea, dizziness, dyspnoea, drowsiness, fast and/or weak pulse, miosis, hypercoagulability, loss of consciousness, nausea and vomiting, numbness and coldness of the extremities, pain in the chest, peripheral vasoconstriction, respiratory depression, rise or fall in blood pressure, severe cramping of the uterus, tachycardia, tingling, and unusual thirst.

Pharmacology Of Enprofylline

Indication	Used in the management of symptoms of asthma. Also used in the treatment of peripheral vascular diseases and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy.
Pharmacodynamics	Enprofylline is a synthetic dimethylxanthine derivative structurally related to theophylline and caffeine. It antagonizes erythrocyte phosphodiesterase, increasing cAMP activity.
Mechanism of action	Enprofylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, enprofylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity.
Absorption	Rapidly absorbed from the digestive tract
Volume of distribution	Not Available
Protein binding	49%
Metabolism	Not Available
Route of elimination	Not Available
Half life	1.9 hours
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Edrophonium

Indication	For the differential diagnosis of myasthenia gravis and as an adjunct in the evaluation of treatment requirements in this disease. It may also be used for evaluating emergency treatment in myasthenic crises.
Pharmacodynamics	Edrophonium is a short and rapid-acting anticholinesterase drug. Its effect is manifest within 30 to 60 seconds after injection and lasts an average of 10 minutes. Edrophonium's pharmacologic action is due primarily to the inhibition or inactivation of acetylcholinesterase at sites of cholinergic transmission. Muscarinic receptors are found throughout the body, especially on muscle. Stimulation of these receptors causes to muscle contraction. In myasthenia gravis the body's immune system destroys many of the muscarinic receptors, so that the muscle becomes less responsive to nervous stimulation. Edrophonium chloride increases the amount of acetylcholine at the nerve endings. Increased levels of acetyl choline allow the remaining receptors to function more efficiently.
Mechanism of action	Edrophonium works by prolonging the action acetylcholine, which is found naturally in the body. It does this by inhibiting the action of the enzyme acetylcholinesterase. Acetylcholine stimulates nicotinic and muscarinic receptors. When stimulated, these receptors have a range of effects.
Absorption	Rapidly absorbed.
Volume of distribution	1.6±0.4 L/kg [Adults] 2.2±1.5 L/kg [Children (0.08-10 yrs)] 1.8±1.2 L/kg [Elderly (65-75 yrs)]
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Edrophonium is primarily renally excreted with 67% of the dose appearing in the urine. Hepatic metabolism and biliary excretion have also been demonstrated in animals
Half life	Distribution half-life is 7 to 12 minutes. Elimination half-life is 33 to 110 minutes.
Clearance	6.8 +/- 2. mL/kg/min [Adults] 6.4 +/- 3.9 mL/kg/min [Children (0.08-10 yrs)] 2.9 +/- 1.9 mL/kg/min [Elderly (65-75 yrs)]
Toxicity	With drugs of this type, muscarine-like symptoms (nausea, vomiting, diarrhea, sweating, increased bronchial and salivary secretions and bradycardia) often appear with overdosage (cholinergic crisis).

Pharmacology Of Echothiophate

Indication	For use in the treatment of subacute or chronic angle-closure glaucoma after iridectomy or where surgery is refused or contraindicated.
Pharmacodynamics	Echothiophate Iodide is a potent, long-acting cholinesterase inhibitor used as a miotic in the treatment of glaucoma. Echothiophate iodide will depress both plasma and erythrocyte cholinesterase levels in most patients after a few weeks of eyedrop therapy.
Mechanism of action	Echothiophate Iodide is a long-acting cholinesterase inhibitor for topical use which enhances the effect of endogenously liberated acetylcholine in iris, ciliary muscle, and other parasympathetically innervated structures of the eye. Echothiophate iodide binds irreversibly to cholinesterase, and is long acting due to the slow rate of hydrolysis by cholinesterase. It causes miosis, increase in facility of outflow of aqueous humor, fall in intraocular pressure, and potentiation of accommodation.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Side effects include blurred vision or change in near or distant vision and eye pain.

Pharmacology Of Drospirenone

Indication	For the prevention of pregnancy in women who elect an oral contraceptive.
Pharmacodynamics	Drospirenone differs from other synthetic progestins in that its pharmacological profile in preclinical studies shows it to be closer to the natural progesterone. As such it has anti-mineralocorticoid properties, counteracts the estrogen-stimulated activity of the renin-angiotensin-aldosterone system, and is not androgenic.
Mechanism of action	Progestins such as drospirenone diffuse freely into target cells in the female reproductive tract, mammary gland, hypothalamus, and the pituitary and bind to the progesterone receptor. Once bound to the receptor, progestins slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH surge.
Absorption	Oral bioavailability is approximately 76%.
Volume of distribution	Not Available
Protein binding	97%
Metabolism	Extensively metabolized following oral or intravenous administration. The two major metabolites are inactive and are formed independent of the CYP450 enzyme system. The metabolites are the acid form of drospirenone formed by opening of the lactone ring and the 4,5-dihydro-drospirenone-3-sulfate.
Route of elimination	Not Available
Half life	30 hours
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Drostanolone

Indication	For use in females, for palliation of androgenresponsive recurrent mammary cancer in women who are more than one year but less than five years postmenopausal.
Pharmacodynamics	Dromostanolone is a synthetic androgen, or male hormone, similar to testosterone. Dromostanolone works by attaching itself to androgen receptors; this causes it to interact with the parts of the cell involved in the making of proteins. It may cause an increase in the synthesis of some proteins or a decrease in the synthesis of others. These proteins have a variety of effects, including blocking the growth of some types of breast cancer cells, stimulating cells that cause male sexual characteristics, and stimulating the production of red blood cells.
Mechanism of action	Dromostanolone is a synthetic androgenic anabolic steroid and is approximately 5 times as potent as natural methyltestosterone. Like testosterone and other androgenic hormones, dromostanolone binds to the androgen receptor. This causes downstream genetic transcriptional changes. This ultimately causes retention of nitrogen, potassium, and phosphorus; increases protein anabolism; and decreases amino acid catabolism. The antitumour activity of dromostanolone appears related to reduction or competitive inhibition of prolactin receptors or estrogen receptors or production.
Absorption	Well absorbed following parenteral administration.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Side effects include virilization (masculine traits in women), acne, fluid retention, and hypercalcemia.

Pharmacology Of Valproic Acid

Indication	For treatment and management of seizure disorders, mania, and prophylactic treatment of migraine headache.
Pharmacodynamics	Valproic Acid is an anticonvulsant and mood-stabilizing drug used primarily in the treatment of epilepsy and bipolar disorder. It is also used to treat migraine headaches and schizophrenia. In epileptics, valproic acid is used to control absence seizures, tonic-clonic seizures (grand mal), complex partial seizures, and the seizures associated with Lennox-Gastaut syndrome. Valproic Acid is believed to affect the function of the neurotransmitter GABA (as a GABA transaminase inhibitor) in the human brain. Valproic Acid dissociates to the valproate ion in the gastrointestinal tract. Valproic acid has also been shown to be an inhibitor of an enzyme called histone deacetylase 1 (HDAC1). HDAC1 is needed for HIV to remain in infected cells. A study published in August 2005 revealed that patients treated with valproic acid in addition to highly active antiretroviral therapy (HAART) showed a 75% reduction in latent HIV infection.
Mechanism of action	Valproic Acid binds to and inhibits GABA transaminase. The drug's anticonvulsant activity may be related to increased brain concentrations of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the CNS, by inhibiting enzymes that catabolize GABA or block the reuptake of GABA into glia and nerve endings. Valproic Acid may also work by suppressing repetitive neuronal firing through inhibition of voltage-sensitive sodium channels. It is also a histone deacetylase inhibitor.
Absorption	Rapid absorption from gastrointestinal tract.
Volume of distribution	11 L/1.73 m2 [total valproate] 92 L/1.73 m2 [free valproate]
Protein binding	Concentration-dependent, from 90% at 40 µg/mL to 81.5% at 130 µg/mL.
Metabolism	Valproic Acid is metabolized almost entirely by the liver. In adult patients on monotherapy, 30-50% of an administered dose appears in urine as a glucuronide conjugate. Mitochondrial ß-oxidation is the other major metabolic pathway, typically accounting for over 40% of the dose. Usually, less than 15-20% of the dose is eliminated by other oxidative mechanisms. Less than 3% of an administered dose is excreted unchanged in urine.
Route of elimination	Valproate is metabolized almost entirely by the liver. Less than 3% of an administered dose is excreted unchanged in urine. Mitochondrial ß-oxidation is the other major metabolic pathway, typically accounting for over 40% of the dose.
Half life	9-16 hours
Clearance	total valproate cl=0.56 L/hr/1.73 m2 free valproate cl=4.6 L/hr/1.73 m2 4.8 +/- 0.17 L/hr/1.73 m2 [males, unbound clearance] 4.7+/- 0.07 L/hr/1.73 m2 [females, unbound clearance]
Toxicity	Oral, mouse: LD50 = 1098 mg/kg; Oral, rat: LD50 = 670 mg/kg. Symptoms of overdose may include coma, extreme drowsiness, and heart problems.

Pharmacology Of Diphenidol

Indication	For use in the prevention and symptomatic treatment of peripheral (labyrinthine) vertigo and associated nausea and vomiting that occur in such conditions as Meniere's disease and surgery of the middle and inner ear. Also for the control of nausea and vomiting associated with postoperative states, malignant neoplasms, labyrinthine disturbances, antineoplastic agent therapy, radiation sickness, and infectious diseases.
Pharmacodynamics	Diphenidol is used for control of nausea and vomiting. It has an antivertigo effect on the vestibular apparatus, inhibiting the chemoreceptor trigger zone to control nausea and vomiting, thus preventing motion sickness.
Mechanism of action	The mechanism by which diphenidol exerts its antiemetic and antivertigo effects is not precisely known. It is thought to diminish vestibular stimulation and depress labyrinthine function and as an antimuscarinic agent. An action on the medullary chemoreceptive trigger zone may also be involved in the antiemetic effect. Diphenidol has no significant sedative, tranquilizing, or antihistaminic action. It has a weak peripheral anticholinergic effect.
Absorption	Well absorbed from gastrointestinal tract following oral administration.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	4 hours
Clearance	Not Available
Toxicity	Symptoms of overdose include drowsiness (severe); shortness of breath or troubled breathing; unusual tiredness or weakness (severe).

Pharmacology Of Dimethylthiambutene

Indication	Dimethylthiambutene is an opioid analgesic previously used in moderate pain relief.
Pharmacodynamics	Not Available
Mechanism of action	Not Available
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Dimenhydrinate

Indication	Used for treating vertigo, motion sickness, and nausea associated with pregnancy.
Pharmacodynamics	Dimenhydrinate is an antiemetics drug combination that contains diphenhydramine and theophylline. It is not effective in the treatment of nausea associated with cancer chemotherapy. Dimenhydrinate directly inhibits the stimulation of certain nerves in the brain and inner ear to suppress nausea, vomiting, dizziness, and vertigo. Diphenhydramine and dimenhydinate both reduce vestibular neuronal excitation due to angular or linear acceleration motions.
Mechanism of action	The mechanism by which some antihistamines exert their antiemetic, anti–motion sickness, and antivertigo effects is not precisely known but may be related to their central anticholinergic actions. They diminish vestibular stimulation and depress labyrinthine function. An action on the medullary chemoreceptive trigger zone may also be involved in the antiemetic effect. Dimenhydrinate is a competitive antagonist at the histamine H1 receptor, which is widely distributed in the human brain. Dimenhydrinate's anti-emetic effect is probably due to H1 antagonism in the vestibular system in the brain.
Absorption	Well absorbed after oral administration.
Volume of distribution	Not Available
Protein binding	98 to 99%.
Metabolism	Hepatic (cytochrome P-450 system).
Route of elimination	Not Available
Half life	1 to 4 hours
Clearance	Not Available
Toxicity	Symptoms of overdose include delerium, hallucinations, and excitment. Patients may be violent and confused.

Pharmacology Of Digitoxin

Indication	For the treatment and management of congestive cardiac insufficiency, arrhythmias and heart failure.
Pharmacodynamics	Digitoxin is a cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting (From Martindale, The Extra Pharmacopoeia, 30th ed, p665). Unlike digoxin (which is eliminated from the body via the kidneys), it is eliminated via the liver, so could be used in patients with poor or erratic kidney function. However, it is now rarely used in current UK medical practice. While there have been several controlled trials which have shown digoxin to be effective in a proportion of patients treated for heart failure, there is not the same strong evidence base for digitoxin, although it is presumed to be similarly effective.
Mechanism of action	Digitoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digitoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Hepatic.
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Digitoxin exhibits similar toxic effects to the more-commonly used digoxin, namely: anorexia, nausea, vomiting, diarrhoea, confusion, visual disturbances, and cardiac arrhythmias.

Pharmacology Of Dicyclomine

Indication	For the treatment of functional bowel/irritable bowel syndrome including Colicky abdominal pain; diverticulitis
Pharmacodynamics	Dicyclomine is an anticholinergic drug, a medication that reduces the effect of acetylcholine, a chemical released from nerves that stimulates muscles, by blocking the receptors for acetylcholine on smooth muscle (a type of muscle). It also has a direct relaxing effect on smooth muscle. Dicyclomine is used to treat or prevent spasm in the muscles of the gastrointestinal tract in the irritable bowel syndrome. In addition, Dicyclomine inhibits gastrointestinal propulsive motility and decreases gastric acid secretion and controls excessive pharyngeal, tracheal and bronchial secretions.
Mechanism of action	Action is achieved via a dual mechanism: (1) a specific anticholinergic effect (antimuscarinic) at the acetylcholine-receptor sites and (2) a direct effect upon smooth muscle (musculotropic).
Absorption	Not Available
Volume of distribution	3.65 L/kg [20 mg oral dose]
Protein binding	>99%
Metabolism	Not Available
Route of elimination	The principal route of elimination is via the urine (79.5% of the dose). Excretion also occurs in the feces, but to a lesser extent (8.4%).
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

pharmacology Of Dicumarol

Indication	For decreasing blood clotting. Often used along with heparin for treatment of deep vein thrombosis.
Pharmacodynamics	Dicumarol is an coumarin-like compound found in sweet clover. It is used as an oral anticoagulant and acts by inhibiting the hepatic synthesis of vitamin K-dependent coagulation factors (prothrombin and factors VII, IX, and X). It is also used in biochemical experiments as an inhibitor of reductases.
Mechanism of action	Dicumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	LD50=233 mg/kg (orally in mice); LD50=250 mg/kg (orally in rats)

Pharmacology Of Dibucaine

Indication	For production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks.
Pharmacodynamics	Dibucaine is an amide-type local anesthetic, similar to lidocaine.
Mechanism of action	Local anesthetics block both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions through sodium channel inhibition. This reversibly stabilizes the membrane and inhibits depolarization, resulting in the failure of a propagated action potential and subsequent conduction blockade.
Absorption	In general, ionized forms (salts) of local anesthetics are not readily absorbed through intact skin. However, both nonionized (bases) and ionized forms of local anesthetics are readily absorbed through traumatized or abraded skin into the systemic circulation.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Primarily hepatic.
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Subcutaneous LD50 in rat is 27 mg/kg. Symptoms of overdose include convulsions, hypoxia, acidosis, bradycardia, arrhythmias and cardiac arrest.

Pharmacology Of Dexmedetomidine

Indication	For sedation of initially intubated and mechanically ventilated patients during treatment in an intensive care setting, also used in pain relief; anxiety reduction and analgesia
Pharmacodynamics	Dexmedetomidine activates 2-adrenoceptors, and causes the decrease of sympathetic tone, with attenuation of the neuroendocrine and hemodynamic responses to anesthesia and surgery; it reduces anesthetic and opioid requirements; and causes sedation and analgesia.
Mechanism of action	Dexmedetomidine is a specific and selective alpha-2 adrenoceptor agonist. By binding to the presynaptic alpha-2 adrenoceptors, it inhibits the release if norepinephrine, therefore, terminate the propagation of pain signals. Activation of the postsynaptic alpha-2 adrenoceptors inhibits the sympathetic activity decreases blood pressure and heart rate.
Absorption	Not Available
Volume of distribution	118 L
Protein binding	94%
Metabolism	Hepatic
Route of elimination	A mass balance study demonstrated that after nine days an average of 95% of the radioactivity, following intravenous administration of radiolabeled dexmedetomidine, was recovered in the urine and 4% in the feces. Fractionation of the radioactivity excreted in urine demonstrated that products of N-glucuronidation accounted for approximately 34% of the cumulative urinary excretion. The majority of metabolites are excreted in the urine.
Half life	2 hours
Clearance	39 L/h [Healthy volunteers receiving IV infusion (0.2-0.7 mcg/kg/hr)]
Toxicity	Not Available

Pharmacology Of Desoxycorticosterone Pivalate

Indication	Examined for treatment of adrenocortical insufficiency especially in multiple sclerosis, congenital cerebral palsy, polyarteritis nodosa, and rheumatoid arthritis. Currently only approved in treating cats and dogs for the treatment of Addison's disease.
Pharmacodynamics	Used to treat adrenocortical insufficiency, desoxycorticosterone pivalate is a mineralocorticoid hormone and an analogue of desoxycorticosterone. It primarily acts on the metabolism of sodium, potassium and water. When the drug is given, there is decreased excretion of sodium accompanied by increased excretion of potassium; the concentration of sodium in the blood is thereby increased whereas that of potassium is decreased. There is a concomitant increase in the volume of blood and extracellular fluids, with a fall in hematocrit. It increases the rate of renal tubular absorption of sodium.
Mechanism of action	Desoxycorticosterone Pivalate binds to the mineralocorticoid receptor. Mineralocorticoids are a family of steroids, secreted by the adrenal cortex, necessary for the regulation of a number of metabolic processes including electrolyte regulation. Desoxycorticosterone pivalate exerts its effect through its interaction with the mineralocorticoid receptor (MR), whereby it reacts with the receptor proteins to form a steroid-receptor complex. This complex moves into the nucleus, where it binds to chromatin which results in genetic transcription of cellular DNA to messenger RNA. The steroid hormones appear to induce transcription and synthesis of specific proteins, which produce the physiological effects seen after administration.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	90%
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Symptoms of overdose include polyuria, polydipsia, increased blood volume, edema, and cardiac enlargement.

Pharmacology Of Desonide

Indication	For the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatose.
Pharmacodynamics	Desonide is a synthetic nonfluorinated corticosteroid for topical dermatologic use. The corticosteroids constitute a class of primarily synthetic steroids used topically as anti-inflammatory and antipruritic agents.
Mechanism of action	Like other topical corticosteroids, desonide has anti-inflammatory, antipruritic and vasoconstrictive properties. The drug binds to cytosolic glucocorticoid receptors. This complex migrates to the nucleus and binds to genetic elements on the DNA. This activates and represses various genes. However corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.
Absorption	Topical corticosteroids can be absorbed from normal intact skin, inflammation and/or other disease processes in the skin may increase percutaneous absorption.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Delta1-dihydrotestosterone

Indication	Not Available
Pharmacodynamics	Delta1-dihydrotestosterone binds to the androgen receptor, a nuclear receptor which binds the androgenic hormones testosterone and dihydrotestosterone. Once bound, the receptor/ligand complex localizes to the nucleus and acts as a DNA binding transcription factor, regulating gene expression. In animals, Delta1-dihydrotestosterone stimulates the growth of the prostate as well as the seminal vesicles.
Mechanism of action	Delta1-dihydrotestosterone binds to the androgen receptor, a nuclear receptor which binds the androgenic hormones testosterone and dihydrotestosterone. Once bound, the receptor/ligand complex localizes to the nucleus and acts as a DNA binding transcription factor, regulating gene expression.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Deferasirox

Indication	For the treatment of chronic iron overload due to blood transfusions (transfusional hemosiderosis) in patients 2 years of age and older.
Pharmacodynamics	Deferasirox is an orally active chelator that is selective for iron (as Fe3+). It is a tridentate ligand that binds iron with high affinity in a 2:1 ratio. Although deferasirox has very low affinity for zinc and copper there are variable decreases in the serum concentration of these trace metals after the administration of deferasirox. The clinical significance of these decreases is uncertain.
Mechanism of action	Two molecules of deferasirox are capable of binding to 1 atom of iron. Deferasirox works in treating iron toxicity by binding trivalent (ferric) iron (for which it has a strong affinity), forming a stable complex which is eliminated via the kidneys.
Absorption	The absolute bioavailability (AUC) of deferasirox tablets for oral suspension is 70% compared to an intravenous dose.
Volume of distribution	14.37 ± 2.69 L
Protein binding	Deferasirox is highly (~99%) protein bound almost exclusively to serum albumin.
Metabolism	Hepatic. CYP450-catalyzed (oxidative) metabolism of deferasirox appears to be minor in humans (about 8%). Glucuronidation is the main metabolic pathway for deferasirox, with subsequent biliary excretion.
Route of elimination	Deferasirox and metabolites are primarily (84% of the dose) excreted in the feces. Renal excretion of deferasirox and metabolites is minimal (8% of the administered dose).
Half life	The mean elimination half-life ranged from 8 to 16 hours following oral administration.
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Decitabine

Indication	For treatment of patients with myelodysplastic syndromes (MDS) including previously treated and untreated, de novo and secondary MDS of all French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia) and intermediate-1, intermediate-2, and high-risk International Prognostic Scoring System groups (scores ≥0.5).
Pharmacodynamics	Decitabine is an analogue of the natural nucleoside 2’-deoxycytidine. It functions in the same way as 5-Azacytidine. The antineoplastic activity of this drug is dependent on its intracellular conversion to its 5'-triphosphate metabolite.
Mechanism of action	Decitabine is believed to exert its antineoplastic effects following its conversion to decitabine triphosphate, where the drug directly incorporates into DNA and inhibits DNA methyltransferase, the enzyme that is responsible for methylating newly synthesized DNA in mammalian cells. This results in hypomethylation of DNA and cellular differentiation or apoptosis. Decitabine inhibits DNA methylation in vitro, which is achieved at concentrations that do not cause major suppression of DNA synthesis. Decitabine-induced hypomethylation in neoplastic cells may restore normal function to genes that are critical for the control of cellular differentiation and proliferation. In rapidly dividing cells, the cytotoxicity of decitabine may also be attributed to the formation of covalent adducts between DNA methyltransferase and decitabine that has been incorporated into DNA. Non-proliferating cells are relatively insensitive to decitabine. Decitabine is cell cycle specific and acts peripherally in the S phase of the cell cycle. It does not inhibit the progression of cells from the G1 to S phase.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Plasma protein binding of decitabine is negligible (<1%).
Metabolism	The exact route of elimination and metabolic fate of decitabine is not known in humans. One of the pathways of elimination of decitabine appears to be deamination by cytidine deaminase found principally in the liver but also in granulocytes, intestinal epithelium and whole blood.
Route of elimination	Not Available
Half life	The terminal phase elimination half-life is 0.51 ± 0.31 hours.
Clearance	125 L/h/m2 [Patients receiving 15 mg/m2 3-hr infusion every 8 hours for 3 days] 210 L/h/m2 [20 mg/m2 1-hr infusion daily for 5 days]
Toxicity	There is no known antidote for overdosage with decitabine. Higher doses are associated with increased myelosuppression including prolonged neutropenia and thrombocytopenia.

Pharmacology Of Decamethonium

Indication	For use as a skeletal muscle relaxant
Pharmacodynamics	Decamethonium acts as a depolarizing muscle relaxant or neuromuscular blocking agent. It acts as an agonist of nicotinic acetycholine receptors in the motor endplate and causes depolarization. This class of drugs has its effect at the neuromuscular junction by preventing the effects of acetylcholine. Normally, when a nerve stimulus acts to contract a muscle, it releases acetylcholine. The binding of this acetylcholine to receptors causes the muscle to contract. Muscle relaxants play an important role in anesthesia even though they don't provide any pain relief or produce unconsciousness.
Mechanism of action	Binds to the nicotinic acetycholine receptors (by virtue of its similarity to acetylcholine) in the motor endplate and blocks access to the receptors. In the process of binding, the receptor is actually activated - causing a process known as depolarization. Since it is not degraded in the neuromuscular junction, the depolarized membrance remains depolarized and unresponsive to any other impulse, causing muscle paralysis.
Absorption	Rapidly absorbed.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	LD50=190 mg/kg (orally in mice). Prolonged apnoea, neuromuscular paralysis and cardiac arrest may occur.

Pharmacology Of Dasatinib

Indication	For the treatment of adults with chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia with resistance or intolerance to prior therapy. Also indicated for the treatment of adults with Philadelphia chromosome-positive acute lymphoblastic leukemia with resistance or intolerance to prior therapy.
Pharmacodynamics	Dasatinib is an oral dual BCR/ABL and Src family tyrosine kinase inhibitor
Mechanism of action	Dasatinib, at nanomolar concentrations, inhibits the following kinases: BCR-ABL, SRC family (SRC, LCK, YES, FYN), c-KIT, EPHA2, and PDGFRβ. Based on modeling studies, dasatinib is predicted to bind to multiple conformations of the ABL kinase. In vitro, dasatinib was active in leukemic cell lines representing variants of imatinib mesylate sensitive and resistant disease. Dasatinib inhibited the growth of chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) cell lines overexpressing BCR-ABL. Under the conditions of the assays, dasatinib was able to overcome imatinib resistance resulting from BCR-ABL kinase domain mutations, activation of alternate signaling pathways involving the SRC family kinases (LYN, HCK), and multi-drug resistance gene overexpression.
Absorption	Not Available
Volume of distribution	2505 L
Protein binding	96%
Metabolism	Dasatinib is extensively metabolized in humans, primarily by the cytochrome P450 enzyme 3A4
Route of elimination	Dasatinib is extensively metabolized in humans, primarily by the cytochrome P450 enzyme 3A4. Elimination is primarily via the feces.
Half life	The overall mean terminal half-life of dasatinib is 3-5 hours.
Clearance	Not Available
Toxicity	Acute overdose in animals was associated with cardiotoxicity.

Pharmacology Of Darunavir

Indication	Darunavir, co-administered with ritonavir, and with other antiretroviral agents, is indicated for the treatment of human immunodeficiency virus (HIV) infection in antiretroviral treatment-experienced adult patients, such as those with HIV-1 strains resistant to more than one protease inhibitor.
Pharmacodynamics	Darunavir is an inhibitor of the human immunodeficiency virus (HIV) protease. In studies, the drug, co-administered with ritonavir in combination therapy, significantly reduced viral load and increased CD4 cell counts in this treatment-experienced patient population (Tibotec, 2006, Product Monograph, Prezista 2006). Darunavir is used as an adjunct therapy with low dose ritonavir, which inhibits cytochrome P450 3A (CYP3A) which increases the bioavailability and half life of darunavir.
Mechanism of action	Darunavir is a HIV protease inhibitor which prevents HIV replication by binding to the enzyme's active site, thereby preventing the dimerization and the catalytic activity of the HIV-1 protease. Darunavir selectively inhibits the cleavage of HIV encoded Gag-Pol polyproteins in virus-infected cells, which prevents the formation of mature infectious virus particles. Structual analyses suggests that the close contact that darunavir has with the main chains of the protease active site amino acids (Asp-29 and Asp-30) is an important contributing factor to its potency and wide spectrum of activity against multi-protease inhibitor resistant HIV-1 variants. Darunavir can also adapt to the changing shape of a protease enzyme because of its molecular flexibility. Darunavir is known to bind to two distinct sites on the enzyme: the active site cavity and the surface of one of the flexible flaps in the protease dimer.
Absorption	The absolute oral bioavailability of a single 600 mg dose of darunavir alone and after co-administration with 100 mg ritonavir twice daily was 37% and 82%, respectively.
Volume of distribution	Not Available
Protein binding	Darunavir is approximately 95% bound to plasma proteins. Darunavir binds primarily to plasma alpha 1-acid glycoprotein (AAG).
Metabolism	Hepatic. Darunavir is extensively metabolized by CYP enzymes, primarily by CYP3A.
Route of elimination	Darunavir is primarily metabolized by CYP3A. Darunavir is extensively metabolized by CYP enzymes, primarily by CYP3A. A mass balance study in healthy volunteers showed that after single dose administration of 400 mg 14C-darunavir, co-administered with 100 mg ritonavir, approximately 79.5% and 13.9% of the administered dose of 14C-darunavir was recovered in the feces and urine, respectively.
Half life	The terminal elimination half-life of darunavir was approximately 15 hours when combined with ritonavir.
Clearance	32.8 L/hr [Healthy volunteers receiving intravenous administration of 400 mg of darunavir] 5.9 L/hr [Healthy volunteers receiving intravenous administrations of 400 mg of darunavir and 100 mg of ritonavir twice daily]
Toxicity	Not Available

Pharmacology Of Danazol

Indication	For the treatment of endometriosis and fibrocystic breast disease (in patients unresponsive to simple measures). Also used for the prophylactic treatment of all types of hereditary angioedema in males and females.
Pharmacodynamics	Danazol is a derivative of the synthetic steroid ethisterone, a modified testosterone. It was approved by the U.S. Food and Drug Administration (FDA) as the first drug to specifically treat endometriosis, but its role as a treatment for endometriosis has been largely replaced by the gonadotropin-releasing hormone (GnRH) agonists. Danazol has antigonadotropic and anti-estrogenic activities. Danazol acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties.
Mechanism of action	As a gonadotropin inhibitor, danazol suppresses the pituitary-ovarian axis possibly by inhibiting the output of pituitary gonadotropins. Danazol also depresses the preovulatory surge in output of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), thereby reducing ovarian estrogen production. Danazol may also directly inhibits ovarian steroidogenesis; bind to androgen, progesterone, and glucocorticoid receptors; bind to sex-hormone-binding globulin and corticosteroid-binding globulin; and increases the metabolic clearance rate of progesterone. Another mechanism of action by which danazol may use to facilitate regression of endometriosis is by decreasing IgG, IgM, and IgA concentrations, as well as phospholipid and IgG isotope autoantibodies. In the treatment of endometriosis, as a consequence of suppression of ovarian function, danazol causes both normal and ectopic endometrial tissues to become inactive and atrophic. This leads to anovulation and associated amenorrhea. In fibrocystic breast disease, the exact mechanism of action of danazol is unknown, but may be related to suppressed estrogenic stimulation as a result of decreased ovarian production of estrogen. A direct effect on steroid receptor sites in breast tissue is also possible. This leads to a disappearance of nodularity, relief of pain and tenderness, and possibly changes in the menstrual pattern. In terms of hereditary angioedema, danazol corrects the underlying biochemical deficiency by increasing serum concentrations of the deficient C1 esterase inhibitor, resulting in increased serum concentrations of the C4 component of the complement system. (Source: PharmGKB)
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Hepatic, to principal metabolites, ethisterone and 17-hydroxymethylethisterone.
Route of elimination	Not Available
Half life	Approximately 24 hours.
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Cycrimine

Indication	For treatment and management of Parkinson's disease.
Pharmacodynamics	Cycrimine is a central anticholenergic used in the treatment of the symptoms of Parkinson's disease. It is a drug used to reduce levels of acetylcholine. Acetylcholine is usually in balance with dopamine neurotransmitters, however lower levels of dopamine are present in the brain of patients suffering from Parkinson's disease. By lowering levels of acetylcholine, it is thought that this balance may be restored.
Mechanism of action	Cycrimine binds the muscarinic acetylcholine receptor M1, effectively inhibiting acetylcholine. This decrease in acetylcholine restores the normal dopamine-acetylcholine balance and relieves the symptoms of Parkinson's disease.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	14-21%
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Cyclacillin

Indication	For the treatment of bacterial infections caused by susceptible organisms.
Pharmacodynamics	Cyclacillin, a penicillin, is a cyclohexylamido analog of penicillanic acid. Cyclacillin is more resistant to beta-lactamase hydrolysis than ampicillin, is much better absorbed when given by mouth and, as a result, the levels reached in the blood and in the urine are considerably higher than those obtained with the same dose of ampicillin. Cyclacillin has been replaced by newer penicillin treatments.
Mechanism of action	The bactericidal activity of cyclacillin results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cyclacillin is stable in the presence of a variety of b-lactamases, including penicillinases and some cephalosporinases.
Absorption	Moderately absorbed.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Symptoms of overdose include severe diarrhea, nausea and vomiting.

Pharmacology Of Crotamiton

Indication	For eradication of scabies (Sarcoptes scabiei) and for symptomatic treatment of pruritic skin.
Pharmacodynamics	Crotamiton is usually used to treat pruritis (itching of the skin) caused by scabies or sunburn. Crotamiton relieves itching by producing what is called a counter-irritation. As crotamiton evaporates from the skin, it produces a cooling effect. This cooling effect helps to divert your body's attention away from the itching. Due to this cooling effect it is also effective for the relief of sunburn. The drug is also believed to kill scabies through an unknown mechanism.
Mechanism of action	Crotamiton is an antiparasitic that is toxic to the scabies mite. Crotamiton also relieves itching by producing what is called a counter-irritation. As crotamiton evaporates from the skin, it produces a cooling effect. This cooling effect helps to divert your body's attention away from the itching.
Absorption	10 % absorbed when applied locally.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Cromoglicic acid

Indication	For the management of patients with bronchial asthma. Also used in the treatment of vernal keratoconjunctivitis, vernal conjunctivitis, and vernal keratitis.
Pharmacodynamics	Cromoglicate or cromolyn (USAN), a synthetic compound, inhibits antigen-induced bronchospasms and, hence, is used to treat asthma and allergic rhinitis. Cromoglicate is used as an ophthalmic solution to treat conjunctivitis and is taken orally to treat systemic mastocytosis and ulcerative colitis.
Mechanism of action	Cromoglicate inhibits degranulation of mast cells, subsequently preventing the release of histamine and slow-reacting substance of anaphylaxis (SRS-A), mediators of type I allergic reactions. Cromoglicate also may reduce the release of inflammatory leukotrienes. Cromoglicate may act by inhibiting calcium influx.
Absorption	1%
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	1.3 hours
Clearance	Not Available
Toxicity	Symptoms of overdose include cough, nasal congestion, nausea, sneezing and wheezing.

Pharmacology Of Conivaptan

Indication	For the treatment of euvolemic or hypervolemic hyponatremia (e.g. the syndrome of inappropriate secretion of antidiuretic hormone, or in the setting of hypothyroidism, adrenal insufficiency, pulmonary disorders, etc.) in hospitalized patients.
Pharmacodynamics	Conivaptan is a nonpeptide, dual antagonist of arginine vasopressin (AVP) V1A and V2 receptors. The level of AVP in circulating blood is critical for the regulation of water and electrolyte balance and is usually elevated in both euvolemic and hypervolemic hyponatremia. The AVP effect is mediated through V2 receptors, which are functionally coupled to aquaporin channels in the apical membrane of the collecting ducts of the kidney. These receptors help to maintain plasma osmolality within the normal range by increasing permeability of the renal collecting ducts to water. Vasopressin also causes vasoconstriction through its actions on vascular 1A receptors. The predominant pharmacodynamic effect of conivaptan in the treatment of hyponatremia is through its V2 antagonism of AVP in the renal collecting ducts, an effect that results in aquaresis, or excretion of free water. Conivaptan's antagonist activity on V1A receptors may also cause splanchnic vasodilation, resulting in possible hypotension or variceal bleeding in patients with cirrhosis. The pharmacodynamic effects of conivaptan include increased free water excretion (i.e., effective water clearance [EWC]) generally accompanied by increased net fluid loss, increased urine output, and decreased urine osmolality.
Mechanism of action	Conivaptan is a dual AVP antagonist with nanomolar affinity for human arginine vasopressin V1A and V2 receptors in vitro. This antagonism occurs in the renal collecting ducts, resulting in aquaresis, or excretion of free water.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	99%
Metabolism	CYP3A4 is the sole cytochrome P450 isozyme responsible for the metabolism of conivaptan. Four metabolites have been identified. The pharmacological activity of the metabolites at V1a and V2 receptors ranged from approximately 3-50% and 50-100% that of conivaptan, respectively.
Route of elimination	Not Available
Half life	5 hours
Clearance	Not Available
Toxicity	Although no data on overdosage in humans are available, conivaptan has been administered as a 20 mg loading dose on Day 1 followed by continuous infusion of 80 mg/day for 4 days in hyponatremia patients and up to 120 mg/day for 2 days in CHF patients. No new toxicities were identified at these higher doses, but adverse events related to the pharmacologic activity of conivaptan, e.g. hypotension and thirst, occurred more frequently at these higher doses.

Pharmacology Of Colistimethate

Indication	For the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli, particularly Pseudomonas aeruginosa.
Pharmacodynamics	Colistimethate is a polymyxin antibiotic agent. Originally, colistimethate sodium was thought to be less toxic than polymyxin B; however, if the drugs are administered at comparable doses, their toxicities may be similar. Polymyxins are cationic polypeptides that disrupt the bacterial cell membrane through a detergentlike mechanism. With the development of less toxic agents, such as extended-spectrum penicillins and cephalosporins, parenteral polymyxin use was largely abandoned, except for the treatment of multidrug-resistant pulmonary infections in patients with cystic fibrosis. More recently, however, the emergence of multidrug-resistant gram-negative bacteria, such as Pseudomonas aeruginosa and Acinetobacter baumannii, and the lack of new antimicrobial agents have led to the revived use of the polymyxins.
Mechanism of action	Colistimethate is a surface active agent which penetrates into and disrupts the bacterial cell membrane. Colistimethate is polycationic and has both hydrophobic and lipophilic moieties. It interacts with the bacterial cytoplasmic membrane, changing its permeability. This effect is bactericidal. There is also evidence that polymyxins enter the cell and precipitate cytoplasmic components, primarily ribosomes.
Absorption	Very poor absorption from gastrointestinal tract.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	As 80% of the dose can be recovered unchanged in the urine, and there is no biliary excretion, it can be assumed that the remaining drug is inactivated in the tissues, however the mechanism is unknown.
Route of elimination	Not Available
Half life	2-3 hours following either intravenous or intramuscular administration in adults and in the pediatric population, including premature infants.
Clearance	Not Available
Toxicity	Oral LD50 in rats is 5450 mg/kg. Overdosage with colistimethate can cause neuromuscular blockade characterized by paresthesia, lethargy, confusion, dizziness, ataxia, nystagmus, disorders of speech and apnea. Respiratory muscle paralysis may lead to apnea, respiratory arrest and death.

Pharmacology Of Clidinium

Indication	For the treatment of peptic ulcer disease and also to help relieve abdominal or stomach spasms or cramps due to colicky abdominal pain, diverticulitis, and irritable bowel syndrome.
Pharmacodynamics	Clidinium is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract.
Mechanism of action	Inhibits muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites primarily by inhibiting the M1 muscarinic receptors.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Signs of toxicity include confusion, paralytic ileus, urinary hesitancy/retention, and blurred vision.

Pharmacology Of Clenbuterol

Indication	Used as a bronchodilator in the treatment of asthma patients.
Pharmacodynamics	Clenbuterol is a substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma. Although approved for use in some countries, as of fall, 2006, clenbuterol is not an ingredient of any therapeutic drug approved by the U.S. Food and Drug Administration.
Mechanism of action	Clenbuterol is a Beta(2) agonist similar in some structural respects to salbutamol. Agonism of the beta(2) receptor stimulates adenylyl cyclase activity which ultimately leads to downstream effects of smooth muscle relaxation in the bronchioles.
Absorption	89-98% orally
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	36-39 hours
Clearance	Not Available
Toxicity	Not Available