Description
Stavudine-13C-d3 is intended for use as an internal standard for the quantification of stavudine (Item No. 14975) by GC- or LC-MS. Stavudine is an inhibitor of HIV reverse transcriptase and a derivative of the nucleoside thymidine (Item No. 20519).1 It inhibits HIV-1 replication in human peripheral blood mononuclear cells (PBMCs; EC50 = 8.8 nM). Stavudine reduces the synthesis of HIV-specific antigen in MT-4 cells when used at concentrations ranging from 0.1 to 10 µg/ml and reduces HIV-induced plaque formation in MT-4 cells at 0.05 µg/ml.2 It reduces plasma- and cell-associated viral load in macaques infected with a highly pathogenic isolate of HIV-2.3 Stavudine induces sustained hind paw mechanical allodynia in a rat model of antiretroviral toxic neuropathy (ATN) when administered at a dose of 75 mg/kg twice weekly for five consecutive doses for a cumulative dose of 375 mg/kg.4 Formulations containing stavudine, in combination with other antiretrovirals, have been used in the treatment of HIV-1 infection.WARNING This product is not for human or veterinary use.
References
[1] TAI-SHUN LIN William H P Raymond F Schinazi. Potent and selective in vitro activity of 3’ -deoxythymidin-2’-ene (3’-deoxy-2’,3’-didehydrothymidine) against human immunodeficiency virus[J]. Biochemical pharmacology, 1987, 36 17: Pages 2713-2718. DOI:
10.1016/0006-2952(87)90253-x[2] Y HAMAMOTO. Inhibitory effect of 2’,3’-didehydro-2’,3’-dideoxynucleosides on infectivity, cytopathic effects, and replication of human immunodeficiency virus.[J]. Antimicrobial Agents and Chemotherapy, 1987, 31 6: 907-910. DOI:
10.1128/aac.31.6.907[3] A WATSON. Early postinfection antiviral treatment reduces viral load and prevents CD4+ cell decline in HIV type 2-infected macaques.[J]. AIDS research and human retroviruses, 1997, 13 16: 1375-1381. DOI:
10.1089/aid.1997.13.1375[4] ANDY KUO. Establishment and characterisation of a stavudine (d4T)-induced rat model of antiretroviral toxic neuropathy (ATN) using behavioural and pharmacological methods.[J]. Inflammopharmacology, 2019, 27 2: 387-396. DOI:
10.1007/s10787-018-00551-8
