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Abacavir Sulfate

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(Treatment for HIV & AIDS)

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CAS: 188062-50-2

Manufacturer: GlaxoSmithKline

ZIAGEN is the brand name for abacavir sulfate, a synthetic carbocyclic nucleoside analogue with inhibitory activity against HIV. The chemical name of abacavir sulfate is (1S,cis) -4-[2-amino-6-(cyclopropylamino)-9 H -purin-9-yl]-2-cyclopentene-1-methanol sulfate (salt) (2:1). Abacavir sulfate is the enantiomer with 1S, 4R absolute configuration on the cyclopentene ring.

It has a molecular formula of (C 14 H 18 N 6 O) 2 H 2 SO 4 and a molecular weight of 670.76 daltons. It has the following structural formula:

Abacavir sulfate is a white to off-white solid with a solubility of approximately 77 mg/mL in distilled water at 25C. It has an octanol/water (pH 7.1 to 7.3) partition coefficient (log P ) of approximately 1.20 at 25C.

The meilting point for abacvir sulfate is: 165

DOSAGE AND ADMINISTRATION of Abacavir sulfate:

A Medication Guide and Warning Card that provide information about recognition of hypersensitivity reactions should be dispensed with each new prescription and refill. To facilitate reporting of hypersensitivity reactions and collection of information on each case, an Abacavir Hypersensitivity Registry has been established. Physicians should register patients by calling 1-800-270-0425.

Abacavir may be taken with or without food.

Adults: The recommended oral dose of abacavir for adults is 600 mg daily, administered as either 300 mg twice daily or 600 mg once daily, in combination with other antiretroviral agents.

Adolescents and Pediatric Patients: The recommended oral dose of abacavir for adolescents and pediatric patients 3 months to up to 16 years of age is 8 mg/kg twice daily (up to a maximum of 300 mg twice daily) in combination with other antiretroviral agents.

Dose Adjustment in Hepatic Impairment: The recommended dose of abacavir in patients with mild hepatic impairment (Child-Pugh score 5 to 6) is 200 mg twice daily. To enable dose reduction, abacavir Oral Solution (10 mL twice daily) should be used for the treatment of these patients. The safety, efficacy, and pharmacokinetic properties of abacavir have not been established in patients with moderate to severe hepatic impairment, therefore abacavir is contraindicated in these patients.

What are the possible side effects of abacavir?

. Fatal hypersensitivity reactions, lactic acidosis, and liver damage have been associated with treatment with abacavir. Stop taking abacavir and seek emergency medical attention if you develop a fever; a skin rash; nausea, vomiting, or unusual or unexpected stomach discomfort; weakness and tiredness; sore throat; shortness of breath; cough; weakness in the arms and legs; yellowing of the skin or eyes; or pain in the upper stomach area. Your pharmacist will provide you with a card listing the symptoms; of a hypersensitivity reaction. Carry this card with you and notify your doctor immediately if you develop any of the symptoms listed. If you need to stop taking abacavir for any reason, do not start taking it again without first talking to your doctor. Dangerous, even fatal, allergic reactions have occurred when abacavir has been restarted, even when no symptoms were present before stopping.
. Other, less serious side effects may be more likely to occur. Notify your doctor if you experience
decreased appetite;
headache;
insomnia; or
redistribution of body fat (loss of fat from the arms, legs, and face and increased fat around the neck, breast, and trunk).
. Side effects other than those listed here may also occur. Talk to your doctor about any side effect that seems unusual or that is especially bothersome.

What other drugs will affect abacavir?

. There are no known interactions between abacavir and other medications.
. Talk to your doctor and pharmacist before taking any prescription or over-the-counter medicines, including herbal products, to reduce the possibility of an interaction.

What is abacavir for?

. Abacavir is an antiviral medication. It is in a category of HIV medicines called reverse transcriptase inhibitors. Abacavir inhibits the reproduction of HIV in the body.
. Abacavir is used to treat the human immunodeficiency virus (HIV), which causes the acquired immunodeficiency syndrome (AIDS). Abacavir is not a cure for HIV or AIDS.
. Abacavir may also be used for purposes other than those listed in this medication guide.

MICROBIOLOGY

Mechanism of Action: Abacavir is a carbocyclic synthetic nucleoside analogue. Abacavir is converted intracellularly 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. The lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated. Abacavir is a weak inhibitor of cellular DNA polymerases (alpha), (beta), and (gamma).

Antiviral Activity: The in vitro anti-HIV-1 activity of abacavir was evaluated against a T-cell tropic laboratory strain HIV-1 IIIB in lymphoblastic cell lines, a monocyte/macrophage tropic laboratory strain HIV-1 BaL in primary monocytes/macrophages, and clinical isolates in peripheral blood mononuclear cells. The concentration of drug necessary to inhibit viral replication by 50 percent (IC 50 ) ranged from 3.7 to 5.8 M (1 M = 0.28 mcg/mL) and 0.07 to 1.0 M against HIV-1 IIIB and HIV-1 BaL , respectively, and was 0.26 0.18 M against 8 clinical isolates. The IC 50 values of abacavir against different HIV-1 clades (A-E) ranged from 0.0015 to 1.0 M, and against HIV-2 isolates, from 0.024 to 0.49 M Abacavir had synergistic activity in vitro in combination with amprenavir, nevirapine, and zidovudine, and additive activity in combination with didanosine, lamivudine, stavudine, tenofovir, and zalcitabine. Ribavirin had no effect on the in vitro anti-HIV-1 activity of abacavir.

Resistance: HIV-1 isolates with reduced susceptibility to abacavir have been selected in vitro and were also obtained from patients treated with abacavir. Genetic analysis of isolates from patients failing an abacavir-containing regimen demonstrated that amino acid substitutions K65R, L74V, Y115F, and M184V in HIV-1 RT contributed to abacavir resistance. In a study of therapy-naive adults receiving ZIAGEN 600 mg once daily (n = 384) or 300 mg twice daily (n = 386), in a background regimen of lamivudine 300 mg once daily and efavirenz 600 mg once daily (Study CNA30021), the incidence of virologic failure at 48 weeks was similar between the 2 groups (11% in both arms). Genotypic (n = 38) and phenotypic analyses (n = 35) of virologic failure isolates from this study showed that the RT mutations that emerged during abacavir once-daily and twice-daily therapy were K65R, L74V, Y115F, and M184V/I. The mutation M184V/I was the most commonly observed mutation in virologic failure isolates from patients receiving abacavir once daily (56%, 10/18) and twice daily (40%, 8/20).

Thirty-nine percent (7/18) of the isolates from patients who experienced virologic failure in the abacavir once-daily arm had a >2.5-fold decrease in abacavir susceptibility with a median-fold decrease of 1.3 (range 0.5 to 11) compared with 29% (5/17) of the failure isolates in the twice-daily arm with a median-fold decrease of 0.92 (range 0.7 to 13).

Cross-Resistance: Cross-resistance has been observed among nucleoside reverse transcriptase inhibitors (NRTIs). Recombinant laboratory strains of HIV-1 HXB2 containing multiple abacavir resistance-associated mutations, namely, K65R, L74V, M184V, and Y115F, exhibited cross-resistance to didanosine, emtricitabine, lamivudine, tenofovir, and zalcitabine in vitro. The K65R mutation can confer resistance to abacavir, didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine; the L74V mutation can confer resistance to abacavir, didanosine, and zalcitabine; and the M184V mutation can confer resistance to abacavir, didanosine, emtricitabine, lamivudine, and zalcitabine. An increasing number of thymidine analogue mutations (TAMs: M41L, D67N, K70R, L210W, T215Y/F, K219E/R/H/Q/N) is associated with a progressive reduction in abacavir susceptibility.