ANI Pharmaceuticals(ANIP)
BAUDETTE, MN
CDMO (Contract Manufacturing)Focus: Generics, Contract Manufacturing
ANI Pharmaceuticals is a life sciences company focused on Generics, Contract Manufacturing.
Neurology
Funding Stage
PUBLIC
Open Jobs
0
Products & Portfolio (11)
39 discontinued products not shown
ACEBUTOLOL HYDROCHLORIDE
acebutolol hydrochloride
Post-LOE
ORAL · CAPSULE
CLINICAL PHARMACOLOGY Acebutolol is a cardioselective, β-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. Pharmacodynamics β1-cardioselectivity has been demonstrated in experimental animal studies. In anesthetized dogs and cats, acebutolol is more potent in antagonizing isoproterenol-induced tachycardia (β1) than in antagonizing isoproterenol-induced vasodilatation (β2). In guinea pigs and cats, it is more potent in antagonizing this tachycardia than in antagonizing isoproterenol-induced bronchodilatation (β2). ISA of acebutolol has been demonstrated in catecholamine-depleted rats by tachycardia induced by intravenous administration of this agent. A membrane-stabilizing effect has been detected in animals, but only with high concentrations of acebutolol. Clinical studies have demonstrated β1-blocking activity at the recommended doses by: a) reduction in the resting heart rate and decrease in exercise-induced tachycardia; b) reduction in cardiac output at rest and after exercise; c) reduction of systolic and diastolic blood pressures at rest and post exercise; d) inhibition of isoproterenol-induced tachycardia. The β1-selectivity of acebutolol has also been demonstrated on the basis of the following vascular and bronchial effects: Vascular Effects: Acebutolol has less antagonistic effects on peripheral vascular β2-receptors at rest and after epinephrine stimulation than nonselective β-antagonists. Bronchial Effects: In single-dose studies in asthmatics examining effects of various beta-blockers on pulmonary function, low doses of acebutolol produce less evidence of bronchoconstriction and less reduction of beta2 agonist, bronchodilating effects, than nonselective agents like propranolol but more than atenolol. ISA has been observed with acebutolol in man, as shown by a slightly smaller (about 3 beats per minute) decrease in resting heart rate when compared to equivalent β-blocking doses of propranolol, metoprolol or atenolol. Chronic therapy with acebutolol induced no significant alteration in the blood lipid profile. Acebutolol has been shown to delay AV conduction time and to increase the refractoriness of the AV node without significantly affecting sinus node recovery time, atrial refractory period, or the HV conduction time. The membrane-stabilizing effect of acebutolol is not manifest at the doses used clinically. Significant reductions in resting and exercise heart rates and systolic blood pressures have been observed 1.5 hours after acebutolol administration with maximal effects occurring between 3 and 8 hours post-dosing in normal volunteers. Acebutolol has demonstrated a significant effect on exercise-induced tachycardia 24 to 30 hours after drug administration. There are significant correlations between plasma levels of acebutolol and both the reduction in resting heart rate and the percent of β-blockade of exercise-induced tachycardia. The antihyper
hypertension in adultsthe management of ventricular premature beatsHypertension
1995
30
ARIMIDEX
anastrozole
LOE Approaching
SMORAL · TABLET
Aromatase Inhibitors
advanced breast cancer in postmenopausal women with disease progression following tamoxifen therapybreast cancer
1995
30
ATACAND
candesartan cilexetil
LOE Approaching
ORAL · TABLET
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. Candesartan 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. Candesartan has much greater affinity (>10,000-fold) 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 widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because candesartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Candesartan 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 increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of candesartan on blood pressure.
hypertension in adultschildren 1 to <17 years of ageto lower blood pressure+6 more
1998
30
ATACAND HCT
candesartan cilexetil and hydrochlorothiazide
LOE Approaching
ORAL · TABLET
Mechanism of Action 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. Candesartan 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. Candesartan has much greater affinity (>10,000-fold) 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 widely used in the treatment of hypertension. ACE inhibitors also inhibit the degradation of bradykinin, a reaction also catalyzed by ACE. Because candesartan does not inhibit ACE (kininase II), it does not affect the response to bradykinin. Whether this difference has clinical relevance is not yet known. Candesartan 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 increased plasma renin activity and angiotensin II circulating levels do not overcome the effect of candesartan on blood pressure. Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing excretion of sodium and chloride in approximately equivalent amounts. Indirectly, the diuretic action of hydrochlorothiazide reduces plasma volume, with consequent increases in plasma renin activity, increases in aldosterone secretion, increases in urinary potassium loss, and decreases in serum potassium. The renin-aldosterone link is mediated by angiotensin II, so co‑administration of an angiotensin II receptor antagonist tends to reverse the potassium loss associated with these diuretics. The mechanism of the antihypertensive effect of thiazides is unknown.
hypertensionto lower blood pressureheart failure
2000
30
BACLOFEN
baclofen
Post-LOE
ORAL · SUSPENSION
GABA A Agonists
spasticity resulting from multiple sclerosisparticularly for the relief of flexor spasmsconcomitant pain+4 more
2023
30
BENAZEPRIL HYDROCHLORIDE
benazepril hydrochloride
Post-LOE
ORAL · TABLET
angiotensin-converting enzyme (ACE) in human subjects and in animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. Hypertensive patients treated with benazepril and amlodipine for up to 56 weeks had elevations of serum potassium up to 0.2 mEq/L [see Warnings and Precautions ()] . Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity. In animal studies, benazepril had no inhibitory effect on the vasopressor response to angiotensin II and did not interfere with the hemodynamic effects of the autonomic neurotransmitters acetylcholine, epinephrine, and norepinephrine. ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of amlodipine and benazepril hydrochloride remains to be elucidated. While the mechanism through which benazepril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin aldosterone system, benazepril has an antihypertensive effect even in patients with low-renin hypertension. Amlodipine Amlodipine is a dihydropyridine calcium antagonist (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.
hypertension in patients not adequately controlled on monotherapy with either agent ()hypertension in patients not adequately controlled on monotherapy with either agenthypertension
2004
30
BENAZEPRIL HYDROCHLORIDE AND HYDROCHLOROTHIAZIDE
benazepril hydrochloride and hydrochlorothiazide
Post-LOE
ORAL · TABLET
Mechanism of Action Benazepril and benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and in animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. Hypertensive patients treated with benazepril alone for up to 52 weeks had elevations of serum potassium of up to 0.2 mEq/L. Similar patients treated with benazepril and hydrochlorothiazide for up to 24 weeks had no consistent changes in their serum potassium (see ). Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity. In animal studies, benazepril had no inhibitory effect on the vasopressor response to angiotensin II and did not interfere with the hemodynamic effects of the autonomic neurotransmitters acetylcholine, epinephrine, and norepinephrine. ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of benazepril hydrochloride and hydrochlorothiazide remains to be elucidated. While the mechanism through which benazepril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, benazepril has an antihypertensive effect even in patients with low-renin hypertension. Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing excretion of sodium and chloride in approximately equivalent amounts. Indirectly, the diuretic action of hydrochlorothiazide reduces plasma volume, with consequent increases in plasma renin activity, increases in aldosterone secretion, increases in urinary potassium loss, and decreases in serum potassium. The renin-aldosterone link is mediated by angiotensin, so coadministration of an ACE inhibitor tends to reverse the potassium loss associated with these diuretics. The mechanism of the antihypertensive effect of thiazides is unknown.
hypertension
2004
30
BEXAROTENE
bexarotene
Post-LOE
ORAL · CAPSULE
(RXRα, RXRß, RXRγ). RXRs can form heterodimers with various receptor partners such as retinoic acid receptors (RARs), vitamin D receptor, thyroid receptor, and peroxisome proliferator activator receptors (PPARs). Once activated, these receptors function as transcription factors that regulate the expression of genes that control cellular differentiation and proliferation. Bexarotene inhibits the growth in vitro of some tumor cell lines of hematopoietic and squamous cell origin. It also induces tumor regression in vivo in some animal models. The exact mechanism of action of bexarotene in the treatment of cutaneous T-cell lymphoma (CTCL) is unknown.
cutaneous manifestations of cutaneous T-cell lymphoma in patientslymphoma
2018
30
BRETHINE
terbutaline sulfate
LOE Approaching
ORAL · TABLET
CLINICAL PHARMACOLOGY In vitro and in vivo pharmacologic studies have demonstrated that terbutaline exerts a preferential effect on beta 2 -adrenergic receptors. While it is recognized that beta 2 -adrenergic receptors are the predominant receptors in bronchial smooth muscle, data indicate that there is a population of beta 2 -receptors in the human heart, existing in a concentration between 10% to 50%. The precise function of these receptors has not been established [see ] . In controlled clinical studies in patients given terbutaline sulfate orally, proportionally greater changes occurred in pulmonary function parameters than in heart rate or blood pressure. While this suggests a relative preference for the beta 2 -receptors in man, the usual cardiovascular effects commonly associated with other sympathomimetic agents were also observed with terbutaline sulfate. The pharmacologic effects of beta-adrenergic agonists, including terbutaline, are at least in part attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic 3', 5'-adenosine monophosphate (cAMP). Increased cAMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Controlled clinical studies have shown that terbutaline sulfate relieves bronchospasm in chronic obstructive pulmonary disease by significantly increasing pulmonary function (e.g., an increase of 15% or more in FEV 1 and in FEF 25%-75% ). After administration of terbutaline sulfate tablets, a measurable change in flow rate usually occurs within 30 minutes, and a clinically significant improvement in pulmonary function occurs within 60 to 120 minutes. The maximum effect usually occurs within 120 to 180 minutes. Terbutaline sulfate also produces a clinically significant decrease in airway and pulmonary resistance, which persists for 4 hours or longer. Significant bronchodilator action (as measured by airway resistance, FEF 25%-75% or PEFR) has also been demonstrated for up to 8 hours in some studies. In studies comparing the effectiveness of terbutaline sulfate with that of ephedrine for up to 3 months, both drugs maintained a significant improvement in pulmonary function throughout this period of treatment. Preclinical 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-agonists and methylxanthines were administered concurrently. The clinical significance of these findings is unknown. Pharmacokinetics Oral administration of 5 mg terbutaline sulfate tablets or 5 mg terbutaline sulfate in solution in 17 healthy, adult, male subjects, resulted in mean (SD) peak plasma terbutaline concentration of 8.3 (3.9) and 8.6 (3.6) ng/mL, which were observed at median
asthma
1976
30
CARBAMAZEPINE
carbamazepine
Post-LOE
ORAL · CAPSULE, EXTENDED RELEASE
Mechanism of Action Carbamazepine has demonstrated anticonvulsant properties in rats and mice with electrically and chemically induced seizures. It appears to act by reducing polysynaptic responses and blocking the post-tetanic potentiation. Carbamazepine greatly reduces or abolishes pain induced by stimulation of the infraorbital nerve in cats and rats. It depresses thalamic potential and bulbar and polysynaptic reflexes, including the linguomandibular reflex in cats. Carbamazepine is chemically unrelated to other anticonvulsants or other drugs used to control the pain of trigeminal neuralgia. The mechanism of action remains unknown. The principal metabolite of carbamazepine, carbamazepine-10,11-epoxide, has anticonvulsant activity as demonstrated in several in vivo animal models of seizures. Though clinical activity for the epoxide has been postulated, the significance of its activity with respect to the safety and efficacy of carbamazepine has not been established.
the treatment of the pain associated with true trigeminal neuralgiaEpilepsy
2011
30
CASODEX
bicalutamide
LOE Approaching
ORAL · TABLET
Androgen Receptor Antagonists
1995
30
Pipeline & Clinical Trials
Iluvien Registry Safety Study
Chronic Diabetic Macular Oedema Considered Insufficiently Responsive to Available TherapiesClinical Trials (1)
NCT01998412Iluvien Registry Safety Study
N/AObservational Study to Assess the Effect of Iluvien® in DME Patients Insufficiently Responsive to Av
Diabetic Macular Edema (DME)Clinical Trials (1)
NCT02080091Observational Study to Assess the Effect of Iluvien® in DME Patients Insufficiently Responsive to Available Therapies
N/AMisoprostol 25 µg Vaginal
Cervical RipeningClinical Trials (1)
NCT07121634Cervical Ripening With Misoprostol vs Isosorbide Mononitrate ; A Parallel -Arm Randomized Controlled Trial
N/AFluocinolone Acetonide
Age-Related Macular DegenerationClinical Trials (1)
NCT00695318Fluocinolone Acetonide Intravitreal Inserts in Geographic Atrophy
Phase 2Fluocinolone Acetonide
Macular EdemaClinical Trials (1)
NCT00770770Fluocinolone Acetonide Intravitreal Inserts for Vein Occlusion in Retina
Phase 2fluocinolone acetonide
Diabetic Macular EdemaClinical Trials (1)
NCT00344968Fluocinolone Acetonide Implant Compared to Sham Injection in Patients With Diabetic Macular Edema
Phase 3Yutiq 0.18 MG Drug Implant
UveitisClinical Trials (1)
NCT05486468The Use of Two YUTIQ Versus Sham for Treatment of Chronic Non Infectious Intraocular Inflammation Affecting the Posterior Segment
Phase 3Fluocinolone Acetonide
Diabetic Macular EdemaClinical Trials (1)
NCT01304706Fluocinolone Acetonide in Diabetic Macular Edema (FAME) Extension Study
Phase 3Fluocinolone Acetonide
Diabetic Macular EdemaClinical Trials (1)
NCT00490815Pharmacokinetic and Efficacy Study of Fluocinolone Acetonide Inserts in Patients With Diabetic Macular Edema
Phase 3Phase 4
Clinical Trials (1)
NCT02472366A Non-Randomized, Open-Label, Single Center Phase 4 Study of the Effect and Safety of ILUVIEN® in Chronic Diabetic Macular Edema Patients Considered Insufficiently Responsive to Available Therapies (Laser, Anti-VEGF) With or Without Intravitreal Corticosteroid Therapy
Phase 4fluocinolone acetonide 190 micrograms
Non-infectious Uveitis Affecting the Posterior Segment of the EyeClinical Trials (1)
NCT06539481Open Label Trial Studying the Safety and Effectiveness of ILUVIEN® (190μg) in Children and Adolescents, Who Have Recurrent Non-infectious Uveitis Affecting the Posterior Segment of the Eye.
Phase 4Iluvien 0.19 MG Drug Implant
Diabetic Macular EdemaClinical Trials (1)
NCT04469595A Study of Intravitreal ILUVIEN® Implant as Baseline Therapy in Patients With Early Diabetic Macular Edema (DME)
Phase 4ILUVIEN 0.19 MG
Diabetic Macular Edema (DME)Clinical Trials (1)
NCT02424019Phase 4 IOP Signals Associated With ILUVIEN®
Phase 4Fluocinolone Acetonide Intravitreal Implant 0.18 mg
Uveitis, PosteriorClinical Trials (1)
NCT05322070Fluocinolone Acetonide Intravitreal Implant 0.18 mg in the Treatment of Chronic Non-Infectious Posterior Segment Uveitis
Phase 4Purified Cortophin Gel, 40 U
Gout ArthritisClinical Trials (1)
NCT07346079Purified Cortrophin® Gel Efficacy and Safety Study of 2 Dose Levels in Patients With Acute Gout Flares
Phase 4Open Jobs (0)
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Interview Prep Quick Facts
Portfolio: 250 approved products, 15 clinical trials
Top TAs: Cardiovascular, Neurology, Infectious Diseases
SEC Filings: 2 available
Portfolio Health
Pre-Launch3 (1%)
Peak2 (1%)
LOE Approaching22 (9%)
Post-LOE223 (89%)
250 total products
Therapeutic Area Focus
Cardiovascular
23 marketed
Neurology
21 marketed
Infectious Diseases
6 marketed
Oncology
5 marketed
Immunology
3 marketed
Psychiatry
2 marketed
Nephrology
2 marketed
Respiratory
2 marketed
Marketed
Pipeline