Hetero

India - Hyderabad

Biotechnology

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Focus: APIs, Generics, Biosimilars

Hetero is a life sciences company focused on APIs, Generics, Biosimilars.

Infectious DiseasesOncologyCardiovascularNeurologyHematology

Funding Stage

PUBLIC

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Products & Portfolio (47)

3 discontinued products not shown

[see Microbiology ( )].

human immunodeficiency virus (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

2016

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

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

HIV-1 infection in adultsweighing at least 6 kg

DNA Polymerase Inhibitors

initial episodesthe management of recurrent episodes of genital herpeschickenpox (varicella)

DNA Polymerase Inhibitors

initial episodesthe management of recurrent episodes of genital herpeschickenpox (varicella)

Xanthine Oxidase Inhibitors

symptoms of primarysecondary gout (acute attackstophi+15 more

2023

AMLODIPINE AND OLMESARTAN MEDOXOMIL

amlodipine and olmesartan medoxomil

Post-LOE

ORAL · TABLET

medoxomil. Amlodipine and olmesartan medoxomil tablet is a combination of two antihypertensive drugs: a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker), amlodipine besylate, and an angiotensin II receptor blocker, olmesartan medoxomil. The amlodipine component of amlodipine and olmesartan medoxomil tablets inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle, and the olmesartan medoxomil component of amlodipine and olmesartan medoxomil tablets blocks the vasoconstrictor effects of angiotensin II. Amlodipine. Experimental data suggests that amlodipine binds to both dihydropyridine and nonhydropyridine 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. Olmesartan medoxomil. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT 1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis. An AT 2 receptor is found also in many tissues, but this receptor is not known to be associated with cardiovascular homeostasis. Olmesartan has more than a 12,500-fold greater affinity for the AT 1 receptor than for the AT 2 receptor. Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is a mechanism of many drugs used to treat hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because olmesartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Block

hypertensionaloneother antihypertensive agents+2 more

2025

AMLODIPINE BESYLATE AND VALSARTAN

amlodipine besylate; valsartan

Post-LOE

SMORAL · TABLET

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. Valsartan Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Valsartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT 1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis. There is also an AT 2 receptor found in many tissues, but AT 2 is not known to be associated with cardiovascular homeostasis. Valsartan has much greater affinity (about 20,000-fold) for the AT 1 receptor than for the AT 2 receptor. The increased plasma levels of angiotensin following AT 1 receptor blockade with valsartan may stimulate the unblocked AT 2 receptor. The primary metabolite of valsartan is essentially inactive with an affinity for the AT 1 receptor about one-200 that of valsartan itself. Blockade of the renin-angiotensin system with ACE inhibitors, which inhibit the biosynthesis of angiotensin II from angiotensin I, is widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because valsartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Valsartan does not bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation. Blockade of the angiotensin II receptor inhibits the negative regulatory feedback of angiotensin II on renin secretion, but the resulting increas

hypertensionto lower blood pressure: In patients not adequately controlled on monotherapy ()nonfatal cardiovascular events+7 more

mania, is unclear. However, the efficacy of aripiprazole in the listed indications could be mediated through a combination of partial agonist activity at D 2 and 5-HT 1A receptors and antagonist activity at 5-HT 2A receptors.

Tourette's disorderSchizophrenia

unknown. However, the efficacy of aripiprazole could be mediated through a combination of partial agonist activity at D 2 and 5-HT 1A receptors and antagonist activity at 5-HT 2A receptors. Actions at receptors other than D 2 , 5-HT 1A , and 5-HT 2A may explain some of the other clinical effects of aripiprazole (e.g., the orthostatic hypotension observed with aripiprazole may be explained by its antagonist activity at adrenergic alpha1 receptors).

HIV-1 antiretroviral drug [see Microbiology ( )].

2022

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Interview Prep Quick Facts

Founded: 2023

Portfolio: 180 approved products

Top TAs: Infectious Diseases, Cardiovascular, Neurology

Portfolio Health

Pre-Launch16 (9%)

Post-LOE164 (91%)

180 total products

Therapeutic Area Focus

32 marketed

26 marketed

24 marketed

17 marketed

6 marketed

6 marketed

5 marketed

5 marketed

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