Abacavir

Catalog No.S5215 Batch:S521501

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Technical Data

Formula

C14H18N6O

Molecular Weight 286.33 CAS No. 136470-78-5
Solubility (25°C)* In vitro DMSO 57 mg/mL (199.07 mM)
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description Abacavir is a powerful nucleoside analog reverse transcriptase inhibitor (NRTI) used to treat HIV and AIDS.
Targets
Reverse transcriptase [1]
In vitro Abacavir (ABC) exhibits potent in vitro antiviral activity against wild-type HIV-1 (IC50 4.0 μM, MT-4 cells)[1]. Abacavir induces chromosomal DSBs and thereby kills ATL cells but not non-HTLV-1-infected cells. Once abacavir is incorporated into the cells, it is phosphorylated in a unique stepwise anabolism to be converted to the triphosphated guanine analog carbovir (CBV) and then incorporated into host chromosomal DNA by replicative DNA polymerases, leading to premature termination of DNA replication, collapse of the replication fork, and DSB formation. Abacavir induces S/G2-phase arrest and apoptosis in ED-40515(−) cells, but not in Jurkat cells[2].
In vivo Abacavir efficiently inhibits the growth of ATL cell xenografts in NOD/SCID mice[2]. In adults, Abacavir is rapidly absorbed after oral administration, with peak concentrations occurring 0.63-1 hour after dosing. The absolute bioavailability of abacavir is approximately 83%. Abacavir pharmacokinetics are linear and doseproportional over the range of 300-1200 mg/day. The apparent volume of distribution of abacavir after intravenous administration is approximately 0.86 ± 0.15 L/kg, suggesting that abacavir is distributed to extravascular spaces. Binding to plasma proteins is about 50% and is independent of the plasma abacavir concentration. Abacavir is extensively metabolized by the liver; less than 2% is excreted as unchanged drug in the urine. Abacavir is primarily metabolized via two pathways, uridine diphosphate glucuronyltransferase and alcohol dehydrogenase, resulting in the inactive glucuronide metabolite and the inactive carboxylate metabolite. The terminal elimination half-life of abacavir is approximately 1.5 hours. The antiviral effect of abacavir is due to its intracellular anabolite, carbovirtriphosphate (CBV-TP). Abacavir is not significantly metabolized by cytochrome P450 (CYP) enzymes, nor does it inhibit these enzymes[3].

Protocol (from reference)

Cell Assay:[2]
  • Cell lines

    Jurkat cells

  • Concentrations

    300 μM

  • Incubation Time

    48 h

  • Method

    Jurkat cells transfected with control siRNA or siTDP1 are treated with or without 300 μM ABC for 48 hours. MTS assay is conducted.

Animal Study:[2]
  • Animal Models

    NOD/SCID mice

  • Dosages

    75 mg/kg

  • Administration

    oral

Selleck's Abacavir has been cited by 10 publications

Biological and Structural Analyses of New Potent Allosteric Inhibitors of HIV-1 Integrase [ Antimicrob Agents Chemother, 2023, 67(7):e0046223] PubMed: 37310224
Reverse Transcriptase Inhibition Disrupts Repeat Element Life Cycle in Colorectal Cancer [ Cancer Discov, 2022, candisc.1117.2021] PubMed: 35320348
HOPX Plays a Critical Role in Antiretroviral Drugs Induced Epigenetic Modification and Cardiac Hypertrophy [ Cells, 2021, 10(12)3458] PubMed: 34943964
Defining stable reference genes in HIV latency reversal experiments [ J Virol, 2021, JVI.02305-20] PubMed: 33762410
Antiretroviral Drugs Regulate Epigenetic Modification of Cardiac Cells Through Modulation of H3K9 and H3K27 Acetylation [ Front Cardiovasc Med, 2021, 8:634774] PubMed: 33898535
Differential Interactome Based Drug Repositioning Unraveled Abacavir, Exemestane, Nortriptyline Hydrochloride, and Tolcapone as Potential Therapeutics for Colorectal Cancers [ Front Bioinform, 2021, 1:710591] PubMed: 36303724
SAMHD1 is active in cycling cells permissive to HIV-1 infection [Badia R, et al. Antiviral Res, 2017, 142:123-135] PubMed: 28359840
The thioacetate-ω(γ-lactam carboxamide) HDAC inhibitor ST7612AA1 as HIV-1 latency reactivation agent [Badia R, et al. Antiviral Res, 2015, 123:62-9] PubMed: 26348004
Nucleoside Reverse Transcriptase Inhibitors Suppress Laser-Induced Choroidal Neovascularization in Mice [ Invest Ophthalmol Vis Sci, 2015, 56(12):7122-9] PubMed: 26529046
SAMHD1 specifically affects the antiviral potency of thymidine analog HIV reverse transcriptase inhibitors [Ballana E, et al. Antimicrob Agents Chemother, 2014, 58(8):4804-13] PubMed: 24913159

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.