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    Stavudine (d4T)
    Stavudine (d4T)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1825
    CAS #: 3056-17-5 Purity ≥98%

    Description: Stavudine (also known as BMY-27857, Sanilvudine, NSC 163661, and d4T) is a potent antiretroviral medication of the nucleoside analog reverse transcriptase inhibitor (NARTI) class, it is active against HIV and has been approved for preventing and treating HIV/AIDS. Stavudine alteres the lipid phenotype, decreasing the lipid content and expression of markers involved in lipid metabolism, namely C/EBPalpha, peroxisome proliferator-activated receptor gamma, adipocyte lipid binding protein 2, fatty acid synthase and acetyl-coenzyme A carboxylase. 

    References: AIDS. 2004 Nov 5;18(16):2127-36; Toxicol Appl Pharmacol. 2004 Aug 15;199(1):10-9.

    Related CAS#: 134624-73-0 (Stavudine sodium)

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    Molecular Weight (MW)224.21 
    FormulaC10H12N2O4 
    CAS No.3056-17-5 (free); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 45 mg/mL (200.7 mM) 
    Water: <1 mg/mL
    Ethanol: 15 mg/mL (66.9 mM) 
    Solubility (In vivo)0.5% CMC Na: 30mg/mL 
    Synonymsd4T; BMY-27857, BMY27857, BMY27857, Sanilvudine, NSC 163661; NSC-163661; NSC163661; Stavudine; Stavudinum; Zerit


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    In Vitro

    In vitro activity: Stavudine alteres the lipid phenotype, decreasing the lipid content and expression of markers involved in lipid metabolism, namely C/EBPalpha, peroxisome proliferator-activated receptor gamma, adipocyte lipid binding protein 2, fatty acid synthase and acetyl-coenzyme A carboxylase. Stavudine drives 5-10% of 3T3-F442A cells towards apoptosis, and reduces the lipid content and survival of differentiated 3T3-L1 adipocytes. Stavudine increases mitochondrial mass by two to fourfold, and loweres the mitochondrial membrane potential (JC-1 stain). Stavudine inhibits p24 antigen production by HIV-I in PBMC with EDsos ranging from 0.04 μM to 0.2 μM. Stavudine produces significant mitochondrial dysfunction with a 1.5-fold increase in cellular lactate to pyruvate ratios. Stavudine causes a dose-dependent decrease in mtDNA amplification and a correlative increase in abundance of markers of mitochondrial oxidative stress. Stavudine treatment elevates mitochondrial reactive oxygen species (ROS), enhances mitochondrial oxidative stress, and contributes mechanistically to NRTI-induced toxicity.

    In VivoStavudine (500 mg/kg/day) results in lack of significant oxidative mtDNA lesions (as assessed by long polymerase chain reaction experiments), and normal blood lactate/pyruvate ratios in lean mice. Stavudine (500 mg/kg/day) can decrease hepatic and muscle mtDNA in lean mice and can also cause ketoacidosis during fasting without altering mtDNA. Stavudine (500 mg/kg/day) depletes WAT mtDNA only in obese mice. 
    Animal modelMice were treated for 2 weeks with stavudine d4T (500 mg/kg/day), L-carnitine (200 mg/kg/day) or both drugs concomitantly. Body fatness was assessed by dual energy X-ray absorptiometry, and investigations were performed in plasma, liver, muscle and WAT. D4T reduced the gain of body adiposity, WAT leptin, whole body FAO and plasma ketone bodies, and increased liver triglycerides and plasma aminotransferases with mild ultrastructural abnormalities in hepatocytes
    Formulation & Dosage500 mg/kg/day
    References IDS. 2004 Nov 5;18(16):2127-36; Toxicol Appl Pharmacol. 2004 Aug 15;199(1):10-9; J Pharmacol Exp Ther. 2001 May;297(2):516-23.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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