아바카비르

Pharmaceuticals -> Used in Switzerland

Pharmaceuticals -> Listed in ZINC15

Breast Feeding; Lactation; Milk, Human; Anti-Infective Agents; Antiviral Agents; Anti-HIV Agents; Anti-Retroviral Agents; Reverse Transcriptase Inhibitors

FDA approved drugs -> Active ingredient

EMA approved medicines: Human medicine

Antiretrovirals > Nucleoside/Nucleotide reverse transcriptase inhibitors

Warning

H302 (87.5%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P261, P264, P264+P265, P270, P272, P280, P301+P317, P302+P352, P305+P351+P338, P318, P321, P330, P333+P317, P337+P317, P362+P364, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 40 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Elevations in serum aminotransferase levels above 5 times the upper limit of normal occur in up to 6% of patients on abacavir. These elevations are usually mild, transient and do not require dose adjustment. Clinically apparent hepatotoxicity is rare, but isolated cases [usually anicteric] have been published. The liver injury usually arises in the context of abacavir hypersensitivity syndrome and may be overshadowed by the allergic syndromes of fever, rash and fatigue. The onset is usually within 1 to 3 months of starting abacavir. The serum enzyme pattern can be hepatocellular or cholestatic. Patients typically recover rapidly within 4 weeks of stopping therapy.

The common toxicities of the NRTI class include mitochondrial toxicity, which can present as hepatic steatosis, lipoatrophy, pancreatitis, and peripheral neuropathy. Symptomatic lactic acidosis can also occur, and these patients require monitoring due to an increased risk of mortality. Long-term antiretroviral therapy (ART) patients may experience fat redistribution, also known as lipodystrophy. Clinicians should avoid abacavir in patients with coronary artery disease and those at increased risk of myocardial infarction due to an increased risk of hyperlipidemia and cardiovascular events.

J - Antiinfectives for systemic use

QJ - Antiinfectives for systemic use

J05AF06

Abacavir is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Abacavir is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The concentration of drug necessary to effect viral replication by 50 percent (EC50) ranged from 3.7 to 5.8 μM (1 μM = 0.28 mcg/mL) and 0.07 to 1.0 μM against HIV-1IIIB and HIV-1BaL, respectively, and was 0.26 ± 0.18 μM against 8 clinical isolates. Abacavir had synergistic activity in cell culture in combination with the nucleoside reverse transcriptase inhibitor (NRTI) zidovudine, the non-nucleoside reverse transcriptase inhibitor (NNRTI) nevirapine, and the protease inhibitor (PI) amprenavir; and additive activity in combination with the NRTIs didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine.

Abacavir is a carbocyclic synthetic nucleoside analogue and an antiviral agent. Intracellularly, abacavir is converted by cellular enzymes to the active metabolite carbovir triphosphate, an analogue of deoxyguanosine-5'-triphosphate (dGTP). Carbovir triphosphate inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA. Viral DNA growth is terminated because the incorporated nucleotide lacks a 3'-OH group, which is needed to form the 5′ to 3′ phosphodiester linkage essential for DNA chain elongation.

Hepatic, by alcohol dehydrogenase and glucuronosyltransferase to a 5′-carboxylic acid metabolite and 5′-glucuronide metabolite, respectively. These metabolites have no antiviral activity. Abacavir is not significantly metabolized by cytochrome P450 enzymes.