Humanwell Pharmaceutical

MO - Ballwin

Pharmaceutical1 H-1B visas (FY2023)

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Focus: Anesthetic and pain medications

Humanwell Pharmaceutical is a life sciences company focused on Anesthetic and pain medications.

NeurologyCardiovascularEndocrinologyOncologyNephrology

Funding Stage

PUBLIC

Open Jobs

0

Products & Portfolio (37)

10 discontinued products not shown

AMANTADINE HYDROCHLORIDE

amantadine hydrochloride

ORAL · CAPSULE

CLINICAL PHARMACOLOGY Pharmacodynamics Mechanism of Action Antiviral The mechanism by which amantadine 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 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 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 and the clinical response to therapy has not been established in man. Sensitivity test results, expressed as the concentration of amantadine required to inhibit by 50% the growth of virus (ED 50 ) in tissue culture vary greatly (from 0.1 mcg/mL to 25.0 mcg/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 up to a concentration of 100 mcg/mL. Drug Resistance Influenza A variants with reduced in vitro sensitivity to amantadine 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 and the clinical response to therapy has not been established. Mechanism of Action Parkinson's Disease The mechanism of action of amantadine in the treatment of Parkinson's disease and drug-induced extrapyramidal reactions is not known. Data from earlier animal studies suggest that amantadine may have direct and indirect effects on dopamine neurons. More recent studies have demonstrated that amantadine is a weak, non-competitive NMDA receptor antagonist (Ki = 10 µM). Although amantadine has not been shown to possess direct anticholinergic activity in animal studies, clinically, it exhibits anticholinergic-like side effects such as dry mouth, urinary retention, and constipation. Pharmacokinetics Amantadine is well absorbed orally. Maximum plasma concentrations are directly related to dose for doses up to 200 mg/day. Doses above 200 mg/day may result in a greater than proportional increase in maximum plasma concentrations. It is primarily excreted unchanged in the urine by glomerular filtration and tubular secretion. Eight metabolites of amantadine have been identified in human urine. One metabolite, an N-acetylated compound, was quantified in human urine and accounted for 5 to 15% of the administered dose. Plasma acetylamantadine accounted fo

the treatment of parkinsonismdrug-induced extrapyramidal reactionsthe treatment of uncomplicated respiratory tract illness caused by influenza A virus strains especially+9 more

ORAL · CAPSULE

CLINICAL PHARMACOLOGY Benzonatate capsules act peripherally by anesthetizing the stretch receptors located in the respiratory passages, lungs, and pleura by dampening their activity and thereby reducing the cough reflex at its source. It begins to act within 15 to 20 minutes and its effect lasts for 3 to 8 hours. Benzonatate capsules have no inhibitory effect on the respiratory center in recommended dosage.

BUPROPION HYDROCHLORIDE

bupropion hydrochloride

ORAL · TABLET, EXTENDED RELEASE

extended-release tablets (SR) enhances the ability of patients to abstain from smoking is not known but is presumed to be related to noradrenergic and/or dopaminergic mechanisms. Bupropion is a relatively weak inhibitor of the neuronal reuptake of norepinephrine and dopamine, and does not inhibit the reuptake of serotonin. Bupropion does not inhibit monoamine oxidase.

BUPROPION HYDROCHLORIDE

bupropion hydrochloride

ORAL · TABLET, EXTENDED RELEASE

unknown, as is the case with other antidepressants. However, it is presumed that this action is mediated by noradrenergic and/or dopaminergic mechanisms. Bupropion is a relatively weak inhibitor of the neuronal uptake of norepinephrine and dopamine and does not inhibit monoamine oxidase or the reuptake of serotonin.

major depressive disorder (MDD)defined by the DiagnosticStatistical Manual (DSM)+3 more

BUPROPION HYDROCHLORIDE

bupropion hydrochloride

ORAL · TABLET, EXTENDED RELEASE

and/or dopaminergic mechanisms. Bupropion is a relatively weak inhibitor of the neuronal reuptake of norepinephrine and dopamine and does not inhibit the reuptake of serotonin. Bupropion does not inhibit monoamine oxidase.

major depressive disorder (MDD)defined by the DiagnosticStatistical Manual (DSM)

ORAL · CAPSULE

CLINICAL PHARMACOLOGY Man's natural supply of vitamin D depends mainly on exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D 3 (cholecalciferol). Vitamin D 3 must be metabolically activated in the liver and the kidney before it is fully active as a regulator of calcium and phosphorus metabolism at target tissues. The initial transformation of vitamin D 3 is catalyzed by a vitamin D 3 -25-hydroxylase enzyme (25-OHase) present in the liver, and the product of this reaction is 25-hydroxyvitamin D 3 [25-(OH)D 3 ]. Hydroxylation of 25-(OH)D 3 occurs in the mitochondria of kidney tissue, activated by the renal 25-hydroxyvitamin D 3 -1 alpha-hydroxylase (alpha-OHase), to produce 1,25-(OH) 2 D 3 (calcitriol), the active form of vitamin D 3 . Endogenous synthesis and catabolism of calcitriol, as well as physiological control mechanisms affecting these processes, play a critical role regulating the serum level of calcitriol. Physiological daily production is normally 0.5 to 1.0 mcg and is somewhat higher during periods of increased bone synthesis (e.g., growth or pregnancy). Pharmacodynamics The two known sites of action of calcitriol are intestine and bone. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Additional evidence suggests that calcitriol may also act on the kidney and the parathyroid glands. Calcitriol is the most active known form of vitamin D 3 in stimulating intestinal calcium transport. In acutely uremic rats calcitriol has been shown to stimulate intestinal calcium absorption. The kidneys of uremic patients cannot adequately synthesize calcitriol, the active hormone formed from precursor vitamin D. Resultant hypocalcemia and secondary hyperparathyroidism are a major cause of the metabolic bone disease of renal failure. However, other bone-toxic substances which accumulate in uremia (e.g., aluminum) may also contribute. The beneficial effect of calcitriol in renal osteodystrophy appears to result from correction of hypocalcemia and secondary hyperparathyroidism. It is uncertain whether calcitriol produces other independent beneficial effects. Calcitriol treatment is not associated with an accelerated rate of renal function deterioration. No radiographic evidence of extraskeletal calcification has been found in predialysis patients following treatment. The duration of pharmacologic activity of a single dose of calcitriol is about 3 to 5 days. Pharmacokinetics Absorption Calcitriol is rapidly absorbed from the intestine. Peak serum concentrations (above basal values) were reached within 3 to 6 hours following oral administration of single doses of 0.25 to 1.0 mcg of calcitriol. Following a single oral dose of 0.5 mcg, mean serum concentrations of calcitriol rose from a baseline value of 40.0 ± 4.4 (SD) pg/mL to 60.0 ± 4.4 pg/mL at 2 hours, and declined to 53.0 ± 6.9 at 4 hours, 50 ± 7.0 at 8 hours, 44 ± 4.6 at 12 hours, and 41.5 ± 5.1 at 24 hours

the management of secondary hyperparathyroidismresultant metabolic bone disease in patients with moderate to severe chronic renal failure (C cr 15 to 55 mL/min) not yet on dialysisthe management of hypocalcemia+4 more

ORAL · TABLET, 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

DESVENLAFAXINE SUCCINATE

desvenlafaxine succinate

ORAL · TABLET, EXTENDED RELEASE

12.1 Mechanism of Action The exact mechanism of the antidepressant action of desvenlafaxine is unknown, but is thought to be related to the potentiation of serotonin and norepinephrine in the central nervous system, through inhibition of their reuptake. Non-clinical studies have shown that desvenlafaxine is a potent and selective serotonin and norepinephrine reuptake inhibitor (SNRI). 12.2 Pharmacodynamics Desvenlafaxine lacked significant affinity for numerous receptors, including muscarinic-cholinergic, H 1 -histaminergic, or a 1 -adrenergic receptors in vitro. Desvenlafaxine also lacked monoamine oxidase (MAO) inhibitory activity. ECG changes Electrocardiograms were obtained from 1,492 desvenlafaxine treated patients with major depressive disorder and 984 placebo-treated patients in clinical studies lasting up to 8 weeks. No clinically relevant differences were observed between desvenlafaxine treated and placebo-treated patients for QT, QTc, PR, and QRS intervals. In a thorough QTc study with prospectively determined criteria, desvenlafaxine did not cause QT prolongation. No difference was observed between placebo and desvenlafaxine treatments for the QRS interval. 12.3 Pharmacokinetics The single-dose pharmacokinetics of desvenlafaxine are linear and dose-proportional in a dose range of 50 to 600 mg (1 to 12 times the recommended approved dosage) per day. With once-daily dosing, steady-state plasma concentrations are achieved within approximately 4 to 5 days. At steady-state, multiple-dose accumulation of desvenlafaxine is linear and predictable from the single-dose pharmacokinetic profile. Absorption The absolute oral bioavailability of desvenlafaxine after oral administration is about 80%. Effect of Food: Ingestion of a high-fat meal (800 to 1000 calories) increased desvenlafaxine C max about 16% and had no effect on AUC. Distribution Steady-state volume of distribution of desvenlafaxine is 3.4 L/kg. Plasma protein binding of desvenlafaxine is 30% and is independent of drug concentration. Elimination Metabolism: Desvenlafaxine is primarily metabolized by conjugation (mediated by UGT isoforms) and, to a minor extent, through oxidative metabolism. CYP3A4 mediates the oxidative metabolism (N-demethylation) of desvenlafaxine. The CYP2D6 metabolic pathway is not involved. The pharmacokinetics of desvenlafaxine was similar in subjects with CYP2D6 poor and extensive metabolizer phenotype. Excretion: Approximately 45% of desvenlafaxine is excreted unchanged in urine at 72 hours after oral administration. Approximately 19% of the administered dose is excreted as the glucuronide metabolite and < 5% as the oxidative metabolite (N,O-didesmethylvenlafaxine) in urine. Specific Populations No clinically significant differences in the exposures of desvenlafaxine were observed based on ethnicity (White, Black, Hispanic). The effect of intrinsic patient factors on the pharmacokinetics of desvenlafaxine is presented in Figure 1. Drug Interaction Studies Clini

DESVENLAFAXINE SUCCINATE

ORAL · TABLET, EXTENDED RELEASE

unknown, but is thought to be related to the potentiation of serotonin and norepinephrine in the central nervous system, through inhibition of their reuptake. Non-clinical studies have shown that desvenlafaxine is a potent and selective SNRI.

ORAL · CAPSULE

5-alpha Reductase Inhibitors

symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: ( ) improve symptomsreduce the risk of acute urinary retentionreduce the risk of the need for BPH-related surgery+4 more

ergocalciferol capsules,

ORAL · CAPSULE

CLINICAL PHARMACOLOGY The in vivo synthesis of the major biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of ergocalciferol takes place in the liver (to 25-hydroxyvitamin D) and the second in the kidneys (to 1,25-dihydroxyvitamin D). Vitamin D metabolites promote the active absorption of calcium and phosphorus by the small intestine, thus elevating serum calcium and phosphate levels sufficiently to permit bone mineralization. Vitamin D metabolites also mobilize calcium and phosphate from bone and probably increase the reabsorption of calcium and perhaps also of phosphate by the renal tubules. There is a time lag of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active metabolites in the liver and kidneys. Parathyroid hormone is responsible for the regulation of this metabolism in the kidneys.

ORAL · CAPSULE

CLINICAL PHARMACOLOGY Ethosuximide suppresses the paroxysmal three cycle per second spike and wave activity associated with lapses of consciousness which is common in absence (petit mal) seizures. The frequency of epileptiform attacks is reduced, apparently by depression of the motor cortex and elevation of the threshold of the central nervous system to convulsive stimuli.

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Pipeline & Clinical Trials

Impact of CYP3A4*1G Polymorphism on Non-analgesic Effects of Fentanyl in Chinese Han Patients

N/A

Clinical Trials (1)

NCT03869346Impact of CYP3A4*1G Polymorphism on Non-analgesic Effects of Fentanyl in Chinese Han Patients

N/A

Hydromorphone

Acute Chest Pain

Phase 1/2

Clinical Trials (1)

NCT06949059Intravenous Hydromorphone for the Treatment of Acute Pain

Phase 1/2

Remimazolam besylate

Mechanically Ventilated Patients

Phase 2

Clinical Trials (1)

NCT06153498PK/PD Properties and Safety of Remazolam Besylate for Injection in ICU Patients With Impaired Renal Function

Phase 2

Remimazolam besylate

Mechanically Ventilated Patients

Phase 2

Clinical Trials (1)

NCT06124404Step 1 of A Two-step Trial to Evaluate the Effectiveness and Safety of Remimazolam Besylate for Sedation in ICU Patients

Phase 2

Nalbuphine hydrochloride injection

Respiratory Insufficiency

Phase 2/3

Clinical Trials (1)

NCT06785571The Evaluation of the Effectiveness and Safety of Nalbuphine Hydrochloride Injection for Analgesia in ICU Patients: A Multicenter, Randomized, Single-blinded, Parallel, Two-step Trial

Phase 2/3

Remimazolam besylate

Phase 3

Clinical Trials (1)

NCT05782894Step 2 of A Two-step Trial to Evaluate the Effectiveness and Safety of Remimazolam Besylate for Sedation in ICU Patients

Phase 3

Remimazolam Besylate

Phase 3

Clinical Trials (1)

NCT04947345The Availability and Safety Study of Remimazolam Besylate for Injection on Sedation of ERAS Patients

Phase 3

Remifentanil

Critical Illness

Phase 4

Clinical Trials (1)

NCT02635802the Research of Analgesia and Sedation Effect of Remifentanil on ICU Short Operation

Phase 4

Rematazolam Besylate

Emergence Agitation

Phase 4

Clinical Trials (1)

NCT05624424Effect of Rematazolam Besylate, Propofol, and Sevoflurane Perioperative Sedation on Incidence of Emergence Agitation and Hemodynamics in Patients Undergoing Laparoscopic Abdominal Surgery

Phase 4

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Interview Prep Quick Facts

Portfolio: 47 approved products, 9 clinical trials

Top TAs: Neurology, Endocrinology, Cardiovascular

H-1B (2023): 1 approval

Portfolio Health

Pre-Launch2 (4%)

Post-LOE45 (96%)

47 total products

Therapeutic Area Focus

5 marketed

3 marketed

2 marketed

2 marketed

2 marketed

1 marketed

Infectious Diseases

1 marketed

1 marketed

Marketed

Pipeline

Visa Sponsorship

Sponsors Work Visas

H-1B Petitions (FY2023)

1

Approved

0

Denied

100%

Rate

Source: USCIS H-1B Employer Data Hub