Matrix Surgical USA

GA - Newnan

Medical Devices2 H-1B visas (FY2023)

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Focus: Porous high-density polyethylene implants for craniofacial reconstructive and aesthetic surgery

Matrix Surgical USA is a life sciences company focused on Porous high-density polyethylene implants for craniofacial reconstructive and aesthetic surgery.

Infectious DiseasesCardiovascular

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Products & Portfolio (16)

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ABACAVIR SULFATE

abacavir sulfate

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

ABACAVIR SULFATE

abacavir sulfate

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

ABACAVIR SULFATE; LAMIVUDINE

abacavir sulfate; lamivudine

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

HIV-1 infection in adultsweighing at least 6 kg

AMLODIPINE AND OLMESARTAN MEDOXOMIL

amlodipine besylate; olmesartan medoxomil

medoxomil. Amlodipine and olmesartan medoxomil 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 inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle, and the olmesartan medoxomil component of amlodipine and olmesartan medoxomil 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. Blockade of the angiotensin

hypertensionaloneother antihypertensive agents+2 more

ATAZANAVIR SULFATE

atazanavir sulfate

ORAL · CAPSULE

HIV-1 antiretroviral drug [see ] .

ATAZANAVIR SULFATE AND RITONAVIR

atazanavir sulfate; ritonavir

SMORAL · TABLET

HIV-1 antiretroviral drug [see ] .

Efavirenz, emtricitabine and tenofovir disoproxil fumarate is a fixed-dose combination of antiviral drugs EFV, FTC, and TDF [see ].

Efavirenz, emtricitabine and tenofovir disoproxil fumarate is a fixed-dose combination of antiviral drugs EFV, FTC, and TDF [see ].

EFAVIRENZ; EMTRICITABINE; TENOFOVIR DISOPROXIL FUMARATE

efavirenz; emtricitabine; tenofovir disoproxil fumarate

Efavirenz, emtricitabine and tenofovir disoproxil fumarate is a fixed-dose combination of antiviral drugs EFV, FTC, and TDF [see ].

ORAL · CAPSULE

fixed-dose combination of antiviral drugs FTC and TDF [see ] .

at-risk adultsadolescents weighing at least 35 kg for pre-exposure prophylaxis (PrEP) to reduce the risk of sexually acquired HIV-1 infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection in adults+1 more

EMTRICITABINE; TENOFOVIR DISOPROXIL FUMARATE

emtricitabine; tenofovir disoproxil fumarate

fixed-dose combination of antiviral drugs FTC and TDF [see ] .

at-risk adultsadolescents weighing at least 35 kg for pre-exposure prophylaxis (PrEP) to reduce the risk of sexually acquired HIV-1 infectioncombination with other antiretroviral agents for the treatment of HIV-1 infection in adults+1 more

LAMIVUDINE/NEVIRAPINE/ZIDOVUDINE TABLETS

lamivudine; nevirapine; zidovudine

ORAL · TABLET, FOR SUSPENSION

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Interview Prep Quick Facts

Portfolio: 17 approved products

Top TAs: Infectious Diseases, Cardiovascular

H-1B (2023): 2 approvals

Portfolio Health

Pre-Launch16 (94%)

Post-LOE1 (6%)

17 total products

Therapeutic Area Focus

Infectious Diseases

3 marketed

1 marketed

Marketed

Pipeline

Visa Sponsorship

Sponsors Work Visas

H-1B Petitions (FY2023)

2

Approved

1

Denied

67%

Rate

Source: USCIS H-1B Employer Data Hub