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MedChemExpressModel Indinavir sulfate - 157810-81-6

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Indinavir sulfate (MK-639) is an orally active and selective HIV-1 protease inhibitor with a Ki of 0.54 nM for PR. Indinavir sulfate exhibits anticancer activity by inhibiting the activation of MMPs-2 hydrolysis, anti-angiogenesis and inducing apoptosis. Indinavir sulfate is also a SARS-CoV 3CLpro inhibitor[1][2][3][4].
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Indinavir sulfate

MCE China:Indinavir sulfate

Brand:MedChemExpress (MCE)

Cat. No.HY-B0689A

CAS:157810-81-6

Synonyms:MK-639; L735524

Purity:99.97%

Storage:-20°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Shipping:Room temperature in continental US; may vary elsewhere.

Description:Indinavir sulfate (MK-639) is an orally active and selective HIV-1 protease inhibitor with a Ki of 0.54 nM for PR. Indinavir sulfate exhibits anticancer activity by inhibiting the activation of MMPs-2 hydrolysis, anti-angiogenesis and inducing apoptosis. Indinavir sulfate is also a SARS-CoV 3CLpro inhibitor.

In Vitro:Indinavir sulfate (0-50 μM; 18 h) blocks lymphocyte cell cycle in G0/G1 phase in PBMCs cells and impairs lymphoproliferative responses[1]. Indinavir sulfate (40 μM-40 nM; 5 days) inhibits cell invasion and (40 μM-40 nM; 48 h) MMPs-2 activation of the Huh7 and SK-HEP-1 hepatocarcinoma cells in vitro[2].

In Vivo:Indinavir sulfate (70 mg/kg; i.g.; once a day for 3 weeks) inhibits the growth of hepatocarcinoma cells in vivo[2].

IC50 & Target:MMP-2 HIV-1

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References:

[1]. Chavan S, et al. The HIV protease inhibitor Indinavir inhibits cell-cycle progression in vitro in lymphocytes of HIV-infected and uninfected individuals. Blood. 2001 Jul 15;98(2):383-9.  [Content Brief]

[2]. Esposito V, et al. Evaluation of antitumoral properties of the protease inhibitor indinavir in a murine model of hepatocarcinoma. Clin Cancer Res. 2006 Apr 15;12(8):2634-9.  [Content Brief]

[3]. Liu F, et al. Kinetic, stability, and structural changes in high-resolution crystal structures of HIV-1 protease with drug-resistant mutations L24I, I50V, and G73S. J Mol Biol. 2005 Dec 9;354(4):789-800.  [Content Brief]

[4]. Hall DC Jr, et al. A search for medications to treat COVID-19 via in silico molecular docking models of the SARS-CoV-2 spike glycoprotein and 3CL protease. Travel Med Infect Dis. 2020 May-Jun;35:101646.  [Content Brief]

Brand introduction:
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