MUT-A
CAS No. 1591906-37-4
MUT-A ( —— )
Catalog No. M12273 CAS No. 1591906-37-4
MUT-A is a novel potent, HIV-1 Integrase IN-LEDGF allosteric inhibitor, shows potent anti-HIV activity with EC50 of 32 nM and 12 nM for NL4-3 or HxB2 HIV-1 strains, respectively.
Purity : >98% (HPLC)
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Biological Information
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Product NameMUT-A
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NoteResearch use only, not for human use.
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Brief DescriptionMUT-A is a novel potent, HIV-1 Integrase IN-LEDGF allosteric inhibitor, shows potent anti-HIV activity with EC50 of 32 nM and 12 nM for NL4-3 or HxB2 HIV-1 strains, respectively.
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DescriptionMUT-A is a novel potent, HIV-1 Integrase IN-LEDGF allosteric inhibitor, shows potent anti-HIV activity with EC50 of 32 nM and 12 nM for NL4-3 or HxB2 HIV-1 strains, respectively; interferes with the IN-LEDGF interaction during integration, shows no cellular toxicity in MT4 cells at 40 uM; inhibits IN (NL4-3)-LEDGF/p75 interaction with IC50 of 92 nM and promotes IN multimerization with activation constant AC50 of 55 nM; impairs virus maturation and infectivity but without influence on RNA packaging or virus immunoreactivity.
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Synonyms——
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PathwayMicrobiology/Virology
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TargetHIV
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RecptorHIV
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Research Area——
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Indication——
Chemical Information
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CAS Number1591906-37-4
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Formula Weight413.58
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Molecular FormulaC24H31NO3S
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Purity>98% (HPLC)
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Solubility——
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SMILES——
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Chemical Name(S)-2-(tert-butoxy)-2-(4-(4,4-dimethylcyclohex-1-en-1-yl)-2-methyl-5-(pyridin-4-yl)thiophen-3-yl)acetic acid
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
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Apelin-36 (rat, mous...
Endogenous APJ receptor agonist that is secreted by adipocytes. Binds with high affinity to APJ receptors (IC50 = 5.4 nM) and potently inhibits cAMP production in vitro (EC50 = 0.52 nM). Involved in regulation of cardiovascular function, fluid homeostasis and feeding. Blocks entry of some HIV-1 and HIV-2 strains into NP-2/CD4 cells expressing APJ.
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DDX3-IN-16d
A small molecule inhibitor (IC50=0.3 uM) of DEAD-box polypeptide 3 (DDX3).
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HIV p17 Gag 77-85
HIV p17 Gag (77-85) is an attractive target for molecular intervention, because it is involved in the viral replication cycle at both the pre- and postintegration levels. In the present experiments, we targeted p17 by intracellularly expressing a cDNA encoding an Ab to p17.