Atazanavir  (Synonyms: BMS-232632)

Atazanavir (BMS-232632) is a highly selective and orally active HIV-1 protease inhibitor . Atazanavir is a substrate and inhibitor of CYP3A4, and an inhibitor of P-glycoprotein (P-gp). Atazanavir is also a SARS-CoV 3CL^pro inhibitor with an IC₅₀ of 3.49 μM. Atazanavir inhibits cardiac fibrosis, hyperlipidemia and induces malignant glioma death^{[1][2][3][4][5][6][7][8]}.

Atazanavir (1-10 μM, 72 h) attenuates hypoxia induced rat cardiac fibroblasts (rCFs) s proliferation by modulating the HMGB1/TLR 9 pathway^[4].
Atazanavir (1-10 μM, 72 h) inhibits collagen I, collagen III, HMGB1, p-IκBα and p-NF-κB expression levels in rat cardiac fibroblasts^[4].
Atazanavir (1-10 μM, 48 h) inhibits the growth of A, U251, T98G, LN229 cells and induces ESR (endoplasmic reticulum stress response) in U251, T98G, and LN229 cells^[6].
Atazanavir (6.0 μM) elicites Ca2+ transients and blebbing of the plasma membranes of C2C12 skeletal muscle myotubes^[7].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Atazanavir (30 mg/kg, i.g., daily, 4 weeks) reduces collagen deposition and inhibits cardiac remodeling in myocardial infarction (MI) model rats^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

704.86

C₃₈H₅₂N₆O₇

198904-31-3

Solid

White to off-white

O=C(OC)N[C@@H](C(C)(C)C)C(NN(CC1=CC=C(C2=NC=CC=C2)C=C1)C[C@H](O)[C@H](CC3=CC=CC=C3)NC([C@H](C(C)(C)C)NC(OC)=O)=O)=O

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Havlir DV, et al. Atazanavir: new option for treatment of HIV infection. Clin Infect Dis. 2004 Jun 1;38(11):1599-604.  [Content Brief]

  [2]. Wood R. Atazanavir: its role in HIV treatment. Expert Rev Anti Infect Ther. 2008 Dec;6(6):785-96.  [Content Brief]

  [3]. Qi Sun, et al. Bardoxolone and bardoxolone methyl, two Nrf2 activators in clinical trials, inhibit SARS-CoV-2 replication and its 3C-like protease. Signal Transduct Target Ther. 2021 May 29;6(1):212.  [Content Brief]

  [4]. Zhang G, et al. Long-term oral atazanavir attenuates myocardial infarction-induced cardiac fibrosis. Eur J Pharmacol. 2018 Jun 5;828:97-102.  [Content Brief]

  [5]. Fukushima K, et al. Effect of serum lipids on the pharmacokinetics of atazanavir in hyperlipidemic rats. Biomed Pharmacother. 2009 Nov;63(9):635-42.  [Content Brief]

  [6]. Pyrko P, et al. HIV-1 protease inhibitors nelfinavir and atazanavir induce malignant glioma death by triggering endoplasmic reticulum stress. Cancer Res. 2007 Nov 15;67(22):10920-8.  [Content Brief]

  [7]. Alomar FA, et al. Efavirenz, atazanavir, and ritonavir disrupt sarcoplasmic reticulum Ca2+ homeostasis in skeletal muscles. Antiviral Res. 2021 Mar;187:104975.  [Content Brief]

  [8]. Robillard KR, et al. Role of P-glycoprotein in the distribution of the HIV protease inhibitor atazanavir in the brain and male genital tract. Antimicrob Agents Chemother. 2014;58(3):1713-22.  [Content Brief]