Cipla

India - Mumbai

Biotechnology1 H-1B visas (FY2023)

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Focus: Generics, APIs, Formulation

Cipla is a life sciences company focused on Generics, APIs, Formulation.

Infectious DiseasesOncologyCardiovascularHematologyRespiratory

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Products & Portfolio (36)

14 discontinued products not shown

ABACAVIR AND LAMIVUDINE

abacavir; lamivudine

Pre-Launch

ORAL · TABLET, FOR SUSPENSION

HIV-1 [see ] .

human immunodeficiency virus type 1 (HIV-1) infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection

[see Microbiology ()] .

human immunodeficiency virus (HIV-1) infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection

12.1 Mechanism of Action Abacavir is an antiretroviral agent [see ]. 12.3 Pharmacokinetics Pharmacokinetics in Adults The pharmacokinetic properties of abacavir were independent of dose over the range of 300 to 1,200 mg per day. Absorption Following oral administration, abacavir is rapidly absorbed and extensively distributed. The geometric mean absolute bioavailability of the tablet was 83%. Plasma abacavir AUC was similar following administration of the oral solution or tablets. After oral administration of 300 mg twice daily in 20 subjects, the steady-state peak serum abacavir concentration (C max ) was 3.0 ± 0.89 mcg per mL (mean ± SD) and AUC (0-12 h) was 6.02 ± 1.73 mcg•hour per mL. After oral administration of a single dose of 600 mg of abacavir in 20 subjects, C max was 4.26 ± 1.19 mcg per mL (mean ± SD) and AUC ∞ was 11.95 ± 2.51 mcg•hour per mL. Effect of Food Bioavailability of abacavir tablets was assessed in the fasting and fed states with no significant difference in systemic exposure (AUC ∞ ); therefore, abacavir tablets may be administered with or without food. Systemic exposure to abacavir was comparable after administration of abacavir oral solution and abacavir tablets. Therefore, these products may be used interchangeably. Distribution The apparent volume of distribution after IV administration of abacavir was 0.86 ± 0.15 L per kg, suggesting that abacavir distributes into extravascular space. In 3 subjects, the CSF AUC (0-6 h) to plasma abacavir AUC (0-6 h) ratio ranged from 27% to 33%. Binding of abacavir to human plasma proteins is approximately 50% and was independent of concentration. Total blood and plasma drug-related radioactivity concentrations are identical, demonstrating that abacavir readily distributes into erythrocytes. Elimination In single-dose trials, the observed elimination half-life (t 1/2 ) was 1.54 ± 0.63 hours. After intravenous administration, total clearance was 0.80 ± 0.24 L per hour per kg (mean ± SD). Metabolism In humans, abacavir is not significantly metabolized by cytochrome P450 enzymes. The primary routes of elimination of abacavir are metabolism by alcohol dehydrogenase to form the 5′-carboxylic acid and glucuronyl transferase to form the 5′-glucuronide. The metabolites do not have antiviral activity. In vitro experiments reveal that abacavir does not inhibit human CYP3A4, CYP2D6, or CYP2C9 activity at clinically relevant concentrations. Excretion Elimination of abacavir was quantified in a mass balance trial following administration of a 600-mg dose of C-abacavir: 99% of the radioactivity was recovered, 1.2% was excreted in the urine as abacavir, 30% as the 5′-carboxylic acid metabolite, 36% as the 5′-glucuronide metabolite, and 15% as unidentified minor metabolites in the urine. Fecal elimination accounted for 16% of the dose. Specific Populations Patients with Renal Impairment The pharmacokinetic properties of abacavir have not been determined in patients with impaired renal function. Renal

human immunodeficiency virus (HIV-1) infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection

human immunodeficiency virus (HIV-1) infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection

ABACAVIR SULFATE AND LAMIVUDINE

abacavir and lamivudine

Post-LOE

ORAL · TABLET

Nucleoside Reverse Transcriptase Inhibitors

human immunodeficiency virus type 1 (HIV-1) infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection

2017

ABACAVIR SULFATE; LAMIVUDINE

abacavir sulfate; lamivudine

Pre-Launch

ORAL · TABLET, FOR SUSPENSION

fixed-dose combination of the HIV‑1 antiretroviral agents abacavir, dolutegravir, and lamivudine [see Microbiology ()].

HIV-1 infection in adultsweighing at least 6 kg

ABACAVIR, DOLUTEGRAVIR, LAMIVUDINE

abacavir, dolutegravir, lamivudine

Pre-Launch

TABLET

fixed-dose combination of the HIV‑1 antiretroviral agents abacavir, dolutegravir, and lamivudine [see Microbiology ()].

HIV-1 infection in adultsweighing at least 6 kg

ALBUTEROL SULFATE

albuterol sulfate

Post-LOE

INHALATION · AEROSOL, METERED

CLINICAL PHARMACOLOGY Mechanism of Action In vitro studies and in vivo pharmacologic studies have demonstrated that albuterol has a preferential effect on beta 2 -adrenergic receptors compared with isoproterenol. While it is recognized that beta 2 -adrenergic receptors are the predominant receptors on bronchial smooth muscle, data indicate that there is a population of beta 2 -receptors in the human heart existing in a concentration between 10% and 50% of cardiac beta-adrenergic receptors. The precise function of these receptors has not been established. (See section.) Activation of beta 2 -adrenergic receptors on airway smooth muscle leads to the activation of adenylcyclase and to an increase in the intracellular concentration of cyclic-3',5'-adenosine monophosphate (cyclic AMP). This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. Albuterol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles. Albuterol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges. Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from mast cells in the airway. Albuterol has been shown in most clinical trials to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses while producing fewer cardiovascular effects. Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or electrocardiographic changes. Preclinical Intravenous studies in rats with albuterol sulfate have demonstrated that albuterol crosses the blood-brain barrier and reaches brain concentrations amounting to approximately 5% of the plasma concentrations. In structures outside the blood-brain barrier (pineal and pituitary glands), albuterol concentrations were found to be 100 times those in the whole brain. Studies in laboratory animals (minipigs, rodents, and dogs) have demonstrated the occurrence of cardiac arrhythmias and sudden death (with histologic evidence of myocardial necrosis) when beta 2 -agonist and methylxanthines were administered concurrently. The clinical significance of these findings is unknown. Propellant HFA-134a is devoid of pharmacological activity except at very high doses in animals (380‑1300 times the maximum human exposure based on comparisons of AUC values), primarily producing ataxia, tremors, dyspnea, or salivation. These are similar to effects produced by the structurally related chlorofluorocarbons (CFCs), which have been used extensively in metered dose inhalers. In animals and human

children 4 years of ageolder for the treatmentprevention of bronchospasm with reversible obstructive airway disease+1 more

2020

ALBUTEROL SULFATE AND IPRATROPIUM BROMIDE

ipratropium bromide and albuterol sulfate

Post-LOE

INHALATION · SOLUTION

CLINICAL PHARMACOLOGY Ipratropium Bromide and Albuterol Sulfate Inhalation Solution is a combination of the β 2 -adrenergic bronchodilator, albuterol sulfate, and the anticholinergic bronchodilator, ipratropium bromide. Albuterol Sulfate Mechanism of Action : The prime action of β-adrenergic drugs is to stimulate adenyl cyclase, the enzyme that catalyzes the formation of cyclic-3', 5'-adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). The cAMP thus formed mediates the cellular responses. In vitro studies and in vivo pharmacologic studies have demonstrated that albuterol has a preferential effect on β 2 -adrenergic receptors compared with isoproterenol. While it is recognized that β 2 -adrenergic receptors are the predominant receptors in bronchial smooth muscle, recent data indicated that 10% to 50% of the β -receptors in the human heart may be β 2 -receptors. The precise function of these receptors, however, is not yet established. Albuterol has been shown in most controlled clinical trials to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses while producing fewer cardiovascular effects. Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other β-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients. Pharmacokinetics: Albuterol sulfate is longer acting than isoproterenol in most patients by any route of administration, because it is not a substrate for the cellular uptake processes for catecholamine nor for the metabolism of catechol-O-methyl transferase. Instead the drug is conjugatively metabolized to albuterol 4'-O-sulfate. Animal Pharmacology/Toxicology: Intravenous studies in rats with albuterol sulfate have demonstrated that albuterol crosses the blood-brain barrier and reaches brain concentrations amounting to approximately 5% of plasma concentrations. In structures outside of the blood-brain barrier (pineal and pituitary glands), albuterol concentrations were found to be 100 times those found in whole brain. Studies in laboratory animals (minipigs, rodents, and dogs) have demonstrated the occurrence of cardiac arrythmias and sudden death (with histological evidence of myocardial necrosis) when beta-agonists and methyl-xanthines are administered concurrently. The clinical significance of these findings is unknown. Ipratropium Bromide Mechanism of Action: Ipratropium bromide is an anticholinergic (parasympatholytic) agent, which blocks the muscarinic receptors of acetylcholine, and, based on animal studies, appears to inhibit vagally mediated reflexes by antagonizing the action of acetylcholine, the transmitter agent released from the vagus nerve. Anticholinergics prevent the increases in intracellular concentration of cyclic guanosine monophosphate (cGMP), resulting from the interaction of acetylcholine with the muscarinic receptors of bronchial smooth muscle.

bronchospasm associated with COPD in patients requiring more than one bronchodilatorCOPD

action. At the cellular level, alendronate shows preferential localization to sites of bone resorption, specifically under osteoclasts. The osteoclasts adhere normally to the bone surface but lack the ruffled border that is indicative of active resorption. Alendronate does not interfere with osteoclast recruitment or attachment, but it does inhibit osteoclast activity. Studies in mice on the localization of radioactive [H]alendronate in bone showed about 10-fold higher uptake on osteoclast surfaces than on osteoblast surfaces. Bones examined 6 and 49 days after [H]alendronate administration in rats and mice, respectively, showed that normal bone was formed on top of the alendronate, which was incorporated inside the matrix. While incorporated in bone matrix, alendronate is not pharmacologically active. Thus, alendronate must be continuously administered to suppress osteoclasts on newly formed resorption surfaces. Histomorphometry in baboons and rats showed that alendronate treatment reduces bone turnover (i.e., the number of sites at which bone is remodeled). In addition, bone formation exceeds bone resorption at these remodeling sites, leading to progressive gains in bone mass.

osteoporosis in postmenopausal womenglucocorticoid-induced osteoporosis in menwomen receiving glucocorticoids in a daily dosage equivalent to 7+6 more

Endothelin Receptor Antagonists

pulmonary arterial hypertension (PAH) (WHO Group 1) in adult patients: To improve exercise abilitydelay clinical worseninghypertension

(calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects can be detected in vitro but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa=8.6), and its kinetic interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect. Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure. The precise mechanisms by which amlodipine relieves angina have not been fully delineated, but are thought to include the following: Exertional Angina: In patients with exertional angina, amlodipine besylate reduces the total peripheral resistance (after load) against which the heart works and reduces the rate pressure product, and thus myocardial oxygen demand, at any given level of exercise. Vasospastic Angina: Amlodipine besylate has been demonstrated to block constriction and restore blood flow in coronary arteries and arterioles in response to calcium, potassium epinephrine, serotonin, and thromboxane A2 analog in experimental animal models and in human coronary vessels in vitro . This inhibition of coronary spasm is responsible for the effectiveness of amlodipine besylate in vasospastic (Prinzmetal's or variant) angina.

hypertensionto lower blood pressureconfirmed+4 more

2007

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Interview Prep Quick Facts

Portfolio: 154 approved products

Top TAs: Infectious Diseases, Oncology, Cardiovascular

H-1B (2023): 1 approval

Portfolio Health

Pre-Launch42 (27%)

Growth1 (1%)

Peak1 (1%)

LOE Approaching1 (1%)

Post-LOE109 (71%)

154 total products

Therapeutic Area Focus

19 marketed

13 marketed

8 marketed

6 marketed

5 marketed

4 marketed

4 marketed

3 marketed

Marketed

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Sponsors Work Visas

H-1B Petitions (FY2023)

Approved

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100%

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Source: USCIS H-1B Employer Data Hub