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Atazanavir | CAS No: 198904-31-3 | GMP-certified suppliers
A medication that treats HIV-1 infection in adults and pediatric patients, improving virological outcomes when used in combination with other antiretroviral agents.
Therapeutic categories
Amino Acids, Peptides, and ProteinsAnti-HIV AgentsAnti-Infective AgentsAnti-Retroviral AgentsAntiinfectives for Systemic UseAntiviral Agents
Generic name
Atazanavir
Molecule type
small molecule
CAS number
198904-31-3
DrugBank ID
DB01072
Approval status
Approved drug, Investigational drug
ATC code
J05AE08
Primary indications
- Atazanavir is indicated in combination with other antiretroviral agents for the treatment of HIV-1 infection in adults and pediatric patients 3 months of age and older weighing at least 5kg
- Atazanavir is also indicated in combination with [cobicistat] and other antiretrovirals for the treatment of HIV-1 infection in adults and pediatric patients weighing at least 35kg
Product Snapshot
- Atazanavir is formulated as an oral small molecule available in various coated tablets and capsules
- It is primarily used in combination with other antiretroviral agents for the treatment of HIV-1 infection
- The product is approved in key regulatory markets including the US, EU, and Canada
Clinical Overview
Atazanavir (CAS Number 198904-31-3) is a protease inhibitor antiretroviral agent indicated for the treatment of HIV-1 infection. It is approved for use in combination with other antiretroviral drugs in adults and pediatric patients from 3 months of age weighing at least 5 kg, and in combination with the pharmacokinetic enhancer cobicistat for patients weighing at least 35 kg. Since its FDA approval in 2003, atazanavir has been utilized primarily as part of combination antiretroviral therapy regimens to improve virological outcomes.
Pharmacologically, atazanavir is an azapeptide inhibitor of the HIV-1 protease enzyme, a critical viral protease responsible for cleaving the Gag and Gag-Pol polyprotein precursors into mature functional viral proteins. By binding competitively at the protease active site, atazanavir prevents this proteolytic processing, leading to the production of immature, non-infectious viral particles. The inhibitory activity extends across multiple HIV-1 group M subtypes (A, B, C, D, AE, AG, F, G, and J) with a low nanomolar EC50, while activity against HIV-2 is variable and generally less potent. Resistance to atazanavir can arise via specific protease mutations such as I50L, N88S, and I84V, which reduce susceptibility but show limited cross-resistance with other protease inhibitors.
Key pharmacokinetic properties include once-daily oral dosing convenience and a favorable lipid profile compared to other protease inhibitors. Atazanavir undergoes extensive hepatic metabolism primarily via cytochrome P450 3A4 (CYP3A4), and is also a substrate and inhibitor of multiple CYP450 isoenzymes and transporters including P-glycoprotein and organic anion transporting polypeptides (OATP). Dose-dependent, asymptomatic prolongation of the PR interval has been observed, although no significant QTc interval prolongation has been associated with therapeutic or supratherapeutic doses.
Safety considerations include potential drug-drug interactions mediated by CYP450 enzymes and transporters, hypersensitivity reactions, and effects on cardiac conduction. Monitoring is advised, especially when coadministered with other agents affecting cardiac conduction or CYP3A4 substrates.
Atazanavir is supplied as a crystalline or amorphous drug substance meeting stringent pharmaceutical quality standards. For quality assurance in API procurement, attention should be paid to polymorphic form, purity levels, residual solvents, and compliance with pharmacopeial standards and regulatory requirements. Due to its complex metabolism and potential for drug interactions, sourcing from verified manufacturers with comprehensive stability and impurity data is recommended to ensure consistent batch-to-batch performance.
Pharmacologically, atazanavir is an azapeptide inhibitor of the HIV-1 protease enzyme, a critical viral protease responsible for cleaving the Gag and Gag-Pol polyprotein precursors into mature functional viral proteins. By binding competitively at the protease active site, atazanavir prevents this proteolytic processing, leading to the production of immature, non-infectious viral particles. The inhibitory activity extends across multiple HIV-1 group M subtypes (A, B, C, D, AE, AG, F, G, and J) with a low nanomolar EC50, while activity against HIV-2 is variable and generally less potent. Resistance to atazanavir can arise via specific protease mutations such as I50L, N88S, and I84V, which reduce susceptibility but show limited cross-resistance with other protease inhibitors.
Key pharmacokinetic properties include once-daily oral dosing convenience and a favorable lipid profile compared to other protease inhibitors. Atazanavir undergoes extensive hepatic metabolism primarily via cytochrome P450 3A4 (CYP3A4), and is also a substrate and inhibitor of multiple CYP450 isoenzymes and transporters including P-glycoprotein and organic anion transporting polypeptides (OATP). Dose-dependent, asymptomatic prolongation of the PR interval has been observed, although no significant QTc interval prolongation has been associated with therapeutic or supratherapeutic doses.
Safety considerations include potential drug-drug interactions mediated by CYP450 enzymes and transporters, hypersensitivity reactions, and effects on cardiac conduction. Monitoring is advised, especially when coadministered with other agents affecting cardiac conduction or CYP3A4 substrates.
Atazanavir is supplied as a crystalline or amorphous drug substance meeting stringent pharmaceutical quality standards. For quality assurance in API procurement, attention should be paid to polymorphic form, purity levels, residual solvents, and compliance with pharmacopeial standards and regulatory requirements. Due to its complex metabolism and potential for drug interactions, sourcing from verified manufacturers with comprehensive stability and impurity data is recommended to ensure consistent batch-to-batch performance.
Identification & chemistry
| Generic name | Atazanavir |
|---|---|
| Molecule type | Small molecule |
| CAS | 198904-31-3 |
| UNII | QZU4H47A3S |
| DrugBank ID | DB01072 |
Pharmacology
| Summary | Atazanavir is an azapeptide inhibitor targeting the HIV-1 protease enzyme, essential for proteolytic cleavage of viral Gag and Gag-Pol polyproteins. By binding to the protease active site, atazanavir inhibits viral maturation, leading to the production of immature, non-infectious HIV-1 particles. It exhibits selective activity against HIV-1 strains and is not active against HIV-2. |
|---|---|
| Mechanism of action | Atazanavir selectively inhibits the virus-specific processing of viral Gag and Gag-Pol polyproteins in HIV-1 infected cells by binding to the active site of HIV-1 protease, thus preventing the formation of mature virions. Atazanavir is not active against HIV-2. |
| Pharmacodynamics | Atazanavir (ATV) is an azapeptide HIV-1 protease inhibitor (PI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Atazanavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Atazanivir is pharmacologically related but structurally different from other protease inhibitors and other currently available antiretrovirals. Atazanavir exhibits anti-HIV-1 activity with a mean 50% effective concentration (EC50) in the absence of human serum of 2 to 5 nM against a variety of laboratory and clinical HIV-1 isolates grown in peripheral blood mononuclear cells, macrophages, CEM-SS cells, and MT-2 cells. Atazanavir has activity against HIV-1 Group M subtype viruses A, B, C, D, AE, AG, F, G, and J isolates in cell culture. Atazanavir has variable activity against HIV-2 isolates (1.9-32 nM), with EC<sub>50</sub> values above the EC<sub>50</sub> values of failure isolates. Two-drug combination antiviral activity studies with atazanavir showed no antagonism in cell culture with PIs (amprenavir, indinavir, lopinavir, nelfinavir, ritonavir, and saquinavir), NNRTIs (delavirdine, efavirenz, and nevirapine), NRTIs (abacavir, didanosine, emtricitabine, lamivudine, stavudine, tenofovir DF, and zidovudine), the HIV-1 fusion inhibitor enfuvirtide, and two compounds used in the treatment of viral hepatitis, adefovir and ribavirin, without enhanced cytotoxicity. HIV-1 isolates with a decreased susceptibility to atazanavir have been selected in cell culture and obtained from patients treated with atazanavir or atazanavir with ritonavir. HIV-1 isolates with 93- to 183-fold reduced susceptibility to atazanavir from three different viral strains were selected in cell culture for 5 months. The substitutions in these HIV-1 viruses that contributed to atazanavir resistance include I50L, N88S, I84V, A71V, and M46I. Changes were also observed at the protease cleavage sites following drug selection. Recombinant viruses containing the I50L substitution without other major PI substitutions were growth impaired and displayed increased susceptibility in cell culture to other PIs (amprenavir, indinavir, lopinavir, nelfinavir, ritonavir, and saquinavir). The I50L and I50V substitutions yielded selective resistance to atazanavir and amprenavir, respectively, and did not appear to be cross-resistant. Concentration- and dose-dependent prolongation of the PR interval in the electrocardiogram has been observed in healthy subjects receiving atazanavir. In placebo-controlled Study AI424-076, the mean (±SD) maximum change in PR interval from the predose value was 24 (±15) msec following oral dosing with 400 mg of atazanavir (n=65) compared to 13 (±11) msec following dosing with placebo (n=67). The PR interval prolongations in this study were asymptomatic. There is limited information on the potential for a pharmacodynamic interaction in humans between atazanavir and other drugs that prolong the PR interval of the electrocardiogram. Electrocardiographic effects of atazanavir were determined in a clinical pharmacology study of 72 healthy subjects. Oral doses of 400 mg (maximum recommended dosage) and 800 mg (twice the maximum recommended dosage) were compared with placebo; there was no concentration-dependent effect of atazanavir on the QTc interval (using Fridericia’s correction). In 1793 subjects with HIV-1 infection, receiving antiretroviral regimens, QTc prolongation was comparable in the atazanavir and comparator regimens. No atazanavir-treated healthy subject or subject with HIV-1 infection in clinical trials had a QTc interval >500 msec |
Targets
| Target | Organism | Actions |
|---|---|---|
| Human immunodeficiency virus type 1 protease | Human immunodeficiency virus 1 | inhibitor |
ADME / PK
| Absorption | Atazanavir is rapidly absorbed with a T<sub>max</sub> of approximately 2.5 hours. Atazanavir demonstrates nonlinear pharmacokinetics with greater than dose-proportional increases in AUC and C<sub>max</sub> values over the dose range of 200 to 800 mg once daily. A steady state is achieved between Days 4 and 8, with an accumulation of approximately 2.3-fold. Administration of atazanavir with food enhances bioavailability and reduces pharmacokinetic variability. Administration of a single 400-mg dose of atazanavir with a light meal (357 kcal, 8.2 g fat, 10.6 g protein) resulted in a 70% increase in AUC and 57% increase in C<sub>max</sub> relative to the fasting state. Administration of a single 400-mg dose of atazanavir with a high-fat meal (721 kcal, 37.3 g fat, 29.4 g protein) resulted in a mean increase in AUC of 35% with no change in C<sub>max</sub> relative to the fasting state. Administration of atazanavir with either a light or high-fat meal decreased the coefficient of variation of AUC and C<sub>max</sub> by approximately one-half compared to the fasting state. Coadministration of a single 300-mg dose of atazanavir and a 100-mg dose of ritonavir with a light meal (336 kcal, 5.1 g fat, 9.3 g protein) resulted in a 33% increase in the AUC and a 40% increase in both the C<sub>max</sub> and the 24-hour concentration of atazanavir relative to the fasting state. Coadministration with a high-fat meal (951 kcal, 54.7 g fat, 35.9 g protein) did not affect the AUC of atazanavir relative to fasting conditions and the C<sub>max</sub> was within 11% of fasting values. The 24-hour concentration following a high-fat meal was increased by approximately 33% due to delayed absorption; the median T<sub>max</sub> increased from 2.0 to 5.0 hours. Coadministration of atazanavir with ritonavir with either a light or a high-fat meal decreased the coefficient of variation of AUC and C<sub>max</sub> by approximately 25% compared to the fasting state. |
|---|---|
| Half-life | The mean elimination half-life of atazanavir in healthy subjects (n=214) and adult subjects with HIV-1 infection (n=13) was approximately 7 hours at steady state following a dose of 400 mg daily with a light meal. Elimination half-life in hepatically impaired is 12.1 hours (following a single 400 mg dose). |
| Protein binding | Atazanavir is 86% bound to human serum proteins and protein binding is independent of concentration. Atazanavir binds to both alpha-1-acid glycoprotein (AAG) and albumin to a similar extent (89% and 86%, respectively). |
| Metabolism | Atazanavir is extensively metabolized in humans. The major biotransformation pathways of atazanavir in humans consisted of monooxygenation and dioxygenation. Other minor biotransformation pathways for atazanavir or its metabolites consisted of glucuronidation, N-dealkylation, hydrolysis, and oxygenation with dehydrogenation. Two minor metabolites of atazanavir in plasma have been characterized. Neither metabolite demonstrated in vitro antiviral activity. In vitro studies using human liver microsomes suggested that atazanavir is metabolized by CYP3A. |
| Route of elimination | Following a single 400-mg dose of <sup>14</sup>C-atazanavir, 79% and 13% of the total radioactivity was recovered in the feces and urine, respectively. Unchanged drugs accounted for approximately 20% and 7% of the administered dose in the feces and urine, respectively. |
| Volume of distribution | In patients with HIV infection, the volume of distribution of atazanavir was estimated to be 88.3 L. |
| Clearance | In patients with HIV infection, the clearance of atazanavir was estimated to be 12.9 L/hr. |
Formulation & handling
- Atazanavir is a small molecule API formulated primarily for oral administration in coated capsules or tablets.
- Due to low aqueous solubility and high lipophilicity (LogP 4.54), formulation approaches should address dissolution and bioavailability enhancement.
- Administration with food is recommended as food increases absorption and reduces pharmacokinetic variability; this should be considered in formulation design.
Regulatory status
| Lifecycle | The API is marketed in Canada, the US, and the EU, with key patents in Canada and the US expiring between 2017 and 2019, while a later US patent extends protection until 2030, indicating a mature market with ongoing patent coverage in the United States. |
|---|
| Markets | Canada, US, EU |
|---|
Supply Chain
| Supply chain summary | Atazanavir is produced and sourced from multiple packagers, including both originator and generic companies, serving markets in Canada, the US, and the EU. Branded products are distributed primarily in North America and Europe, with patent protection extending in the US until 2030, indicating limited generic competition currently in these regions. The presence of multiple packaging entities suggests an established supply chain that supports both branded and generic formulations where patents have expired or do not apply. |
|---|
Atazanavir is a type of Anti-HIV
The Anti-HIV category of pharmaceutical APIs comprises a range of active pharmaceutical ingredients (APIs) specifically designed to combat the human immunodeficiency virus (HIV). These APIs play a critical role in the development and production of antiretroviral drugs, which are used to treat HIV infections and prevent the progression to acquired immunodeficiency syndrome (AIDS).
Anti-HIV APIs work by targeting various stages of the HIV life cycle, inhibiting viral replication and reducing the viral load in the body. Some commonly used APIs in this category include nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and integrase inhibitors (INIs).
NRTIs, such as tenofovir and emtricitabine, act by blocking the reverse transcriptase enzyme, an essential component in the replication of the virus. NNRTIs, such as efavirenz and nevirapine, bind to the reverse transcriptase enzyme, preventing its proper functioning. PIs, like ritonavir and atazanavir, inhibit the protease enzyme, crucial for viral maturation and assembly. INIs, such as raltegravir and dolutegravir, target the integrase enzyme, impeding viral integration into the host's DNA.
These APIs are carefully synthesized and undergo rigorous quality testing to ensure their safety, efficacy, and compliance with regulatory standards. Pharmaceutical companies utilize these APIs as key building blocks to formulate antiretroviral medications, which are then prescribed to individuals living with HIV/AIDS worldwide.
Overall, the Anti-HIV API category plays a vital role in the ongoing battle against HIV/AIDS, offering effective treatment options and improved quality of life for patients affected by this challenging condition.
