Products & Portfolio (29)
21 discontinued products not shown
AMANTADINE HYDROCHLORIDE
amantadine hydrochloride
Post-LOE
ORAL · SYRUP
Mechanisms of Action: Antiviral The mechanism by which amantadine hydrochloride exerts its antiviral activity is not clearly understood. It appears to mainly prevent the release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. In certain cases, amantadine hydrochloride is also known to prevent virus assembly during virus replication. It does not appear to interfere with the immunogenicity of inactivated influenza A virus vaccine. Antiviral Activity Amantadine hydrochloride inhibits the replication of influenza A virus isolates from each of the subtypes, i.e., H1N1, H2N2 and H3N2. It has very little or no activity against influenza B virus isolates. A quantitative relationship between the in vitro susceptibility of influenza A virus to amantadine hydrochloride and the clinical response to therapy has not been established in man. Sensitivity test results, expressed as the concentration of amantadine hydrochloride required to inhibit by 50% the growth of virus (ED50) in tissue culture vary greatly (from 0.1 µg/mL to 25.0 µg/mL) depending upon the assay protocol used, size of virus inoculum, isolates of influenza A virus strains tested, and the cell type used. Host cells in tissue culture readily tolerated amantadine hydrochloride up to a concentration of 100 µg/mL. Drug Resistance Influenza A variants with reduced in vitro sensitivity to amantadine hydrochloride have been isolated from epidemic strains in areas where adamantane derivatives are being used. Influenza viruses with reduced in vitro sensitivity have been shown to be transmissible and to cause typical influenza illness. The quantitative relationship between the in vitro sensitivity of influenza A variants to amantadine hydrochloride and the clinical response to therapy has not been established.
the treatment of parkinsonismdrug-induced extrapyramidal reactionsthe treatment of uncomplicated respiratory tract illness caused by influenza A virus strains especially+9 more
1995
30
AMIODARONE HYDROCHLORIDE
amiodarone hydrochloride
Post-LOE
INJECTION · INJECTABLE
drug, but it possesses electrophysiologic characteristics of all four Vaughan Williams classes. Like class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies, and like class II drugs, amiodarone exerts a noncompetitive antisympathetic action. One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness. The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Its vasodilatory action can decrease cardiac workload and consequently myocardial oxygen consumption. Intravenous amiodarone administration prolongs intranodal conduction (Atrial-His, AH) and refractoriness of the atrioventricular node (ERP AVN), but has little or no effect on sinus cycle length (SCL), refractoriness of the right atrium and right ventricle (ERP RA and ERP RV), repolarization (QTc), intraventricular conduction (QRS), and infra-nodal conduction (His-ventricular, HV). A comparison of the electrophysiologic effects of intravenous amiodarone and oral amiodarone is shown in the table below. Table 6: EFFECTS OF INTRAVENOUS AND ORAL AMIODARONE ON ELECTROPHYSIOLOGIC PARAMETERS Formulation SCL QRS QTc AH HV ERP RA ERP RV ERP AVN ↔ No change Intravenous ↔ ↔ ↔ ↑ ↔ ↔ ↔ ↑ Oral ↑ ↔ ↑ ↑ ↔ ↑ ↑ ↑ At higher doses (> 10 mg/kg) of intravenous amiodarone, prolongation of the ERP RV and modest prolongation of the QRS have been seen. These differences between oral and IV administration suggest that the initial acute effects of intravenous amiodarone may be predominately focused on the AV node, causing an intranodal conduction delay and increased nodal refractoriness due to slow channel blockade (class IV activity) and noncompetitive adrenergic antagonism (class II activity).
2024
30
AMLODIPINE BESYLATE AND BENAZEPRIL HYDROCHLORIDE
amlodipine besylate and benazepril hydrochloride
Post-LOE
ORAL · CAPSULE
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
2010
30
AMLODIPINE BESYLATE; BENAZEPRIL HYDROCHLORIDE
amlodipine besylate and benazepril hydrochloride
Post-LOE
ORAL · CAPSULE
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
2010
30
APIXABAN
apixaban
Pre-Launch
ORAL · TABLET
FXa. It does not require antithrombin III for antithrombotic activity. Apixaban inhibits free and clot-bound FXa, and prothrombinase activity. Apixaban has no direct effect on platelet aggregation, but indirectly inhibits platelet aggregation induced by thrombin. By inhibiting FXa, apixaban decreases thrombin generation and thrombus development.
deep vein thrombosis (DVT)which may lead to pulmonary embolism (PE)knee replacement surgery+10 more
BROMPHENIRAMINE MALEATE, PSEUDOEPHEDRINE HYDROCHLORIDE AND DEXTROMETHORPHAN HYDROBROMIDE
brompheniramine maleate, pseudoephedrine hydrochloride, and dextromethorphan hydrobromide
Post-LOE
ORAL · SYRUP
CLINICAL PHARMACOLOGY Brompheniramine maleate is a histamine antagonist, specifically an H1-receptor-blocking agent belonging to the alkylamine class of antihistamines. Antihistamines appear to compete with histamine for receptor sites on effector cells. Brompheniramine also has anticholinergic (drying) and sedative effects. Among the antihistaminic effects, it antagonizes the allergic response (vasodilation, increased vascular permeability, increased mucus secretion) of nasal tissue. Brompheniramine is well absorbed from the gastrointestinal tract, with peak plasma concentration after single, oral dose of 4 mg reached in 5 hours; urinary excretion is the major route of elimination, mostly as products of biodegradation; the liver is assumed to be the main site of metabolic transformation. Pseudoephedrine acts on sympathetic nerve endings and also on smooth muscle, making it useful as a nasal decongestant. The nasal decongestant effect is mediated by the action of pseudoephedrine on α-sympathetic receptors, producing vasoconstriction of the dilated nasal arterioles. Following oral administration, effects are noted within 30 minutes with peak activity occurring at approximately one hour. Dextromethorphan acts centrally to elevate the threshold for coughing. It has no analgesic or addictive properties. The onset of antitussive action occurs in 15 to 30 minutes after administration and is of long duration.
2014
30
CARBAMAZEPINE
carbamazepine
Post-LOE
ORAL · TABLET, EXTENDED RELEASE
Cytochrome P450 3A4 Inducers
the treatment of the pain associated with true trigeminal neuralgiaEpilepsy
2022
30
CEFACLOR
cefaclor
Post-LOE
ORAL · FOR SUSPENSION
CLINICAL PHARMACOLOGY Cefaclor is well-absorbed after oral administration to fasting subjects. Total absorption is the same whether the drug is given with or without food; however, when it is taken with food, the peak concentration achieved is 50% to 75% of that observed when the drug is administered to fasting subjects and generally appears from three-fourths to 1 hour later. Following administration of 250 mg, 500 mg, and 1 g doses to fasting subjects, average peak serum levels of approximately 7, 13, and 23 mcg/mL, respectively, were obtained within 30 to 60 minutes. Approximately 60% to 85% of the drug is excreted unchanged in the urine within 8 hours, the greater portion being excreted within the first 2 hours. During this 8-hour period, peak urine concentrations following the 250 mg, 500 mg and 1 g doses were approximately 600, 900 and 1,900 mcg/mL, respectively. The serum half-life in normal subjects is 0.6 to 0.9 hour. In patients with reduced renal function, the serum half-life of cefaclor is slightly prolonged. In those with complete absence of renal function, the plasma half-life of the intact molecule is 2.3 to 2.8 hours. Excretion pathways in patients with markedly impaired renal function have not been determined. Hemodialysis shortens the half-life by 25% to 30%. Microbiology Mechanism of Action As with other cephalosporins, the bactericidal action of cefaclor results from inhibition of cell-wall synthesis. Mechanism of Resistance Resistance to cefaclor is primarily through hydrolysis of beta-lactamases, alteration of penicillin-binding proteins (PBPs) and decreased permeability. Pseudomonas spp., Acinetobacter calcoaceticus and most strains of Enterococci (Enterococcus faecalis , group D streptococci), Enterobacter spp., indole-positive Proteus, Morganella morganii (formerly Proteus morganii), Providencia rettgeri (formerly Proteus rettgeri ), and Serratia spp. are resistant to cefaclor. Cefaclor is inactive against methicillin-resistant staphylococci. β-lactamase-negative, ampicillin-resistant strains of H. influenzae should be considered resistant to cefaclor despite apparent in vitro susceptibility to this agent. Antibacterial Activity Cefaclor has been shown to be active against most strains of the following microorganisms both in vitro and in clinical infections as described in the section. Gram-positive Bacteria Staphylococcus aureus (methicillin susceptible only) Coagulase negative staphylococci (methicillin susceptible only) Streptococcus pneumoniae Streptococcus pyogenes (group A β-hemolytic streptococci) Gram-negative Bacteria Escherichia coli Haemophilus influenzae (excluding β-lactamase-negative, ampicillin-resistant strains) Klebsiella spp. Proteus mirabilis The following in vitro data are available, but their clinical significance is unknown. At least 90 percent of the following bacteria exhibit an in vitro minimum inhibitory concentrations (MICs) less than or equal to the susceptible breakpoint of cefaclor. However,
the treatment of the following infectionsHaemophilus influenzaestaphylococci+2 more
2012
30
CEFACLOR
cefaclor
Post-LOE
ORAL · CAPSULE
CLINICAL PHARMACOLOGY Cefaclor is well absorbed after oral administration to fasting subjects. Total absorption is the same whether the drug is given with or without food; however, when it is taken with food, the peak concentration achieved is 50% to 75% of that observed when the drug is administered to fasting subjects and generally appears from three fourths to 1 hour later. Following administration of 250-mg, 500-mg, and 1-g doses to fasting subjects, average peak serum levels of approximately 7, 13, and 23 mcg/mL respectively were obtained within 30 to 60 minutes. Approximately 60% to 85% of the drug is excreted unchanged in the urine within 8 hours, the greater portion being excreted within the first 2 hours. During this 8-hour period, peak urine concentrations following the 250-mg, 500-mg and 1-g doses were approximately 600, 900 and 1,900 mc g/mL, respectively. The serum half-life in normal subjects is 0.6 to 0.9 hour. In patients with reduced renal function, the serum half-life of cefaclor is slightly prolonged. In those with complete absence of renal function, the plasma half-life of the intact molecule is 2.3 to 2.8 hours. Excretion pathways in patients with markedly impaired renal function have not been determined. Hemodialysis shortens the half-life by 25% to 30%. Microbiology Mechanism of Action As with other cephalosporins, the bactericidal action of cefaclor results from inhibition of cell-wall synthesis. Mechanism of Resistance Resistance to cefaclor is primarily through hydrolysis of beta-lactamases, alteration of penicillin-binding proteins (PBPs) and decreased permeability. Pseudomonas spp ., Acinetobacter calcoaceticus and most strains of Enterococi ( Enterococcus faecalis, group D streptococci), Enterobacter spp ., indole-positive Proteus, Morganella morganii (formerly Proteus morganii ), Providencia rettgeri (formerly Proteus rettgeri ) and Serratia spp. are resistant to cefaclor. Cefaclor is inactive against methicillin-resistant staphylococci. β-lactamase-negative, ampicillin-resistant strains of H. influenzae should be considered resistant to cefaclor despite apparent in vitro susceptibility to this agent. Antibacterial Activity Cefaclor has been shown to be active against most strains of the following microorganisms both in vitro and in clinical infections as described in the INDICATIONS AND USAGE section. Gram-positive Bacteria Staphylococcus aureus (methicillin susceptible only) Coagulase negative staphylococci (methicillin susceptible only) Streptococcus pneumoniae Streptococcus pyogenes (group A β-hemolytic streptococci) Gram-negative Bacteria Escherichia coli Haemophilus influenzae (excluding β-lactamase-negative, ampicillin-resistant strains) Klebsiella spp. Proteus mirabilis The following in vitro data are available, but their clinical significance is unknown . At least 90 percent of the following bacteria exhibit an in vitro minimum inhibitory concentrations (MICs) less than or equal to the susceptible breakpoint
the treatment of the following infectionsHaemophilus influenzaestaphylococci+2 more
2004
30
CEPHALEXIN
cephalexin
Post-LOE
ORAL · FOR SUSPENSION
12.1 Mechanism of Action Cephalexin is a cephalosporin antibacterial drug [see Microbiology ( )] . 12.3 Pharmacokinetics Absorption: Cephalexin is acid stable and may be given without regard to meals. Following doses of 250 mg, 500 mg, and 1 g, average peak serum levels of approximately 9, 18, and 32 mcg/mL, respectively, were obtained at 1 hour. Serum levels were detectable 6 hours after administration (at a level of detection of 0.2 mcg/mL). Distribution: Cephalexin is approximately 10% to 15% bound to plasma proteins. Excretion: Cephalexin is excreted in the urine by glomerular filtration and tubular secretion. Studies showed that over 90% of the drug was excreted unchanged in the urine within 8 hours. During this period, peak urine concentrations following the 250 mg, 500 mg, and 1 g doses were approximately 1000, 2200, and 5000 mcg/mL respectively. Drug Interactions In healthy subjects given single 500 mg doses of cephalexin and metformin, plasma metformin mean C max and AUC increased by an average of 34% and 24%, respectively, and metformin mean renal clearance decreased by 14%. No information is available about the interaction of cephalexin and metformin following multiple doses of either drug. 12.4 Microbiology Mechanism of Action Cephalexin is a bactericidal agent that acts by the inhibition of bacterial cell-wall synthesis. Resistance Methicillin-resistant staphylococci and most isolates of enterococci are resistant to cephalexin. Cephalexin is not active against most isolates of Enterobacter spp., Morganella morganii , and Proteus vulgaris . Cephalexin has no activity against Pseudomonas spp., or Acinetobacter calcoaceticus . Penicillin-resistant Streptococcus pneumoniae is usually cross-resistant to beta-lactam antibacterial drugs. Antimicrobial Activity Cephalexin has been shown to be active against most isolates of the following bacteria both in vitro and in clinical infections [ see Indications and Usage ( ) ]. Gram-positive bacteria Staphylococcus aureus (methicillin-susceptible isolates only) Streptococcus pneumoniae (penicillin-susceptible isolates) Gram-negative bacteria Escherichia coli Haemophilus influenzae Klebsiella pneumoniae Moraxella catarrhalis Proteus mirabilis Susceptibility Tests For specific information regarding susceptibility test interpretive criteria and associated test methods and quality control standards recognized by FDA for this drug, please see: .
the following infections caused by susceptible isolates of designated bacteria: Respiratory tract infection ( ) Otitis media ( ) Skinskin structure infections ( ) Bone infections ( ) Genitourinary tract infections ( ) To reduce the development of drug-resistant bacteriamaintain the effectiveness of Cephalexin for oral suspension+18 more
2007
30
CETIRIZINE HYDROCHLORIDE
cetirizine hydrochloride
Post-LOE
ORAL · SOLUTION
Mechanism of Actions Cetirizine, a human metabolite of hydroxyzine, is an antihistamine; its principal effects are mediated via selective inhibition of peripheral H 1 receptors. The antihistaminic activity of cetirizine has been clearly documented in a variety of animal and human models. In vivo and ex vivo animal models have shown negligible anticholinergic and antiserotonergic activity. In clinical studies, however, dry mouth was more common with cetirizine than with placebo. In vitro receptor binding studies have shown no measurable affinity for other than H 1 receptors. Autoradiographic studies with radiolabeled cetirizine in the rat have shown negligible penetration into the brain. Ex vivo experiments in the mouse have shown that systemically administered cetirizine does not significantly occupy cerebral H 1 receptors.
the uncomplicated skin manifestations of chronic idiopathic urticaria in children 6 months to 5 years of age
2008
30
CHLORHEXIDINE GLUCONATE
chlorhexidine gluconate
Post-LOE
DENTAL · SOLUTION
CLINICAL PHARMACOLOGY Chlorhexidine gluconate oral rinse, 0.12% provides antimicrobial activity during oral rinsing. The clinical significance of chlorhexidine gluconate oral rinse, 0.12% antimicrobial activities is not clear. Microbiological sampling of plaque has shown a general reduction of counts of certain assayed bacteria, both aerobic and anaerobic, ranging from 54-97% through six months use. Use of chlorhexidine gluconate oral rinse in a six month clinical study did not result in any significant changes in bacteria resistance, overgrowth of potentially opportunistic organisms or other adverse changes in the oral microbial ecosystem. Three months after chlorhexidine gluconate oral rinse use was discontinued, the number of bacteria in plaque had returned to baseline levels and resistance of plaque bacteria to chlorhexidine gluconate was equal to that at baseline. Pharmacokinetics Pharmacokinetic studies with chlorhexidine gluconate oral rinse indicate approximately 30% of the active ingredient, chlorhexidine gluconate, is retained in the oral cavity following rinsing. This retained drug is slowly released into the oral fluids. Studies conducted on human subjects and animals demonstrate chlorhexidine gluconate is poorly absorbed from the gastrointestinal tract. The mean plasma level of chlorhexidine gluconate reached a peak of 0.206 µg/g in humans 30 minutes after they ingested a 300 mg dose of the drug. Detectable levels of chlorhexidine gluconate were not present in the plasma of these subjects 12 hours after the compound was administered. Excretion of chlorhexidine gluconate occurred primarily through the feces (~90%). Less than 1% of the chlorhexidine gluconate ingested by these subjects was excreted in the urine.
1995
30
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Interview Prep Quick Facts
Founded: 2013
Portfolio: 111 approved products
Top TAs: Neurology, Infectious Diseases, Immunology
H-1B (2023): 1 approval
Portfolio Health
Pre-Launch10 (9%)
Launch2 (2%)
Peak2 (2%)
LOE Approaching4 (4%)
Post-LOE93 (84%)
111 total products
Therapeutic Area Focus
Neurology
16 marketed
Infectious Diseases
14 marketed
Immunology
8 marketed
Cardiovascular
6 marketed
Respiratory
5 marketed
Psychiatry
3 marketed
Musculoskeletal
3 marketed
Gastroenterology
2 marketed
Marketed
Pipeline
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H-1B Petitions (FY2023)
1
Approved
0
Denied
100%
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Source: USCIS H-1B Employer Data Hub