BMMP
BMMP is an anti-HIV-1 agent and hnRNP M modulator. BMMP modulates hnRNP M function to suppress CD44 mRNA expression. BMMP induces abnormal uncoating of the HIV viral core at the post-entry step. BMMP suppresses migration of TGF-β-stimulated lung carcinoma cells. BMMP suppresses HIV-1 reverse transcription and replication without inhibiting virion release. BMMP exerts anti-HIV-1 activity via a mechanism distinct from CA protein-binding heterocyclic compounds. BMMP can be used for the research of human immunodeficiency virus infection and non-small cell lung cancer.
For research use only. We do not sell to patients.
- CAS No.: 748785-70-8
- Formula: C13H11N3S2
- Molecular Weight:273.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
BMMP (20 μM; 2 d) does not reduce the viability of 293T or M8166 cells[1].
BMMP (20 μM; 3 d) inhibits full-cycle HIV-1 replication across 293T and M8166 cells to 30% of control levels[1].
BMMP (20 μM) does not affect the release of HIV-1 virions from 293T cells[1].
BMMP (20 μM; 1 d) does not significantly alter the infectivity of HIV-1 virions produced by 293T cells[1].
BMMP (20 μM; 1 d) potently inhibits early-phase HIV-1 infectivity in M8166 cells to less than 10% of control levels[1].
BMMP (20 μM; 2 d) does not affect HIV-1 reverse transcription but suppresses nuclear localization and integration of viral DNA in 293T cells, reducing 2-LTR DNA to 60% and Alu-LTR DNA to 46% of control levels[1].
BMMP (20 μM; 1 d) destabilizes HIV-1 CA protein in infected HeLa cells[1].
BMMP (20 μM; 1 d) does not change the nuclear localization of hnRNP M but reduces HIV-1 CA protein levels in infected HeLa cells[1].
BMMP (20 μM; 1 d) inhibits early-phase HIV-1 infectivity in both control and hnRNP M-knockdown HeLa cells, indicating hnRNP M is not involved in BMMP's anti-HIV activity[1].
BMMP (0.1-100 μM; 2 d) at 0.1-50 μM does not reduce A549 cell viability, while 100 μM BMMP shows mild toxicity[1].
BMMP (0.1-100 μM; 24 h total incubation with TGF-β stimulation) inhibits TGF-β-induced migration of A549 cells in a concentration-dependent manner, with near-complete inhibition at 20 μM[1].
BMMP (20 μM; 1 h, 3 h, 6 h, or 1 d incubation with TGF-β stimulation) slightly reduces vimentin mRNA levels but does not inhibit TGF-β-induced EMT marker changes in A549 cells[1].
BMMP (20 μM; 1 d incubation with TGF-β stimulation) reduces TGF-β-induced increases in CD44s, CD44v8, and CD44v10 mRNA levels in A549 cells[1].
BMMP (20 μM; 1 d incubation with TGF-β stimulation) reduces TGF-β-induced CD44 mRNA expression in A549 cells via hnRNP M, as the effect is abolished in hnRNP M-knockdown cells[1].
BMMP (20 μM; up to 100 hours) inhibits replication of HIV-1 NL4-3 strain in human T-lymphoblastoid M8166 cells[2].
BMMP does not directly interact with HIV-1 Pr55Gag or CA protein in a cell-free surface plasmon resonance assay[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human kidney cell line 293T, human T-lymphoblastoid cell line M8166
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Concentration:20 μM
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Incubation Time:2 d
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Result:Showed no significant toxicity to 293T or M8166 cells.
Maintained relative cell viability at ~100% compared to untreated controls.
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Cell Line:HeLa cells infected with HIV-1
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Concentration:20 μM
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Incubation Time:1 d
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Result:Destabilized the HIV-1 CA (p24) protein, reducing its detectable levels compared to untreated controls.
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Cell Line:HeLa cells infected with HIV-1
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Concentration:20 μM
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Incubation Time:1 d
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Result:Did not alter the nuclear localization of hnRNP M.
Reduced detectable p24 (CA) protein levels.
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Cell Line:human lung carcinoma cell line A549
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Concentration:0.1 μM; 0.5 μM; 1 μM; 5 μM; 20 μM; 50 μM; 100 μM
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Incubation Time:2 d
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Result:At 0.1-50 μM did not significantly reduce A549 cell viability (relative viability ~90-105% of control).
At 100 μM caused a slight reduction to ~85% of control.
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Cell Line:TGF-β-stimulated human lung carcinoma cell line A549
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Concentration:0.1 μM; 0.5 μM; 1 μM; 5 μM; 20 μM; 50 μM; 100 μM
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Incubation Time:24 h total incubation with TGF-β stimulation
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Result:Inhibited TGF-β-induced A549 cell migration in a concentration-dependent manner.
Reduced migration by ~50% at 0.5 μM.
Nearly completely inhibited migration at 20 μM.
Maintained significant inhibitory activity at 100 μM.
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Cell Line:TGF-β-stimulated human lung carcinoma cell line A549
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Concentration:20 μM
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Incubation Time:1 h, 3 h, 6 h, or 1 d incubation with TGF-β stimulation
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Result:Did not alter E-cadherin mRNA levels.
Slightly reduced vimentin mRNA levels at 1 d post-TGF-β stimulation.
Did not significantly reduce N-cadherin, snail, or fibronectin mRNA levels after 1 d of TGF-β stimulation.
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Cell Line:TGF-β-stimulated human lung carcinoma cell line A549
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Concentration:20 μM
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Incubation Time:1 d incubation with TGF-β stimulation
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Result:Reduced TGF-β-induced increases in CD44s, CD44v8, and CD44v10 mRNA levels in A549 cells.
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Cell Line:TGF-β-stimulated human lung carcinoma cell line A549 (hnRNP M-knockdown)
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Concentration:20 μM
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Incubation Time:1 d incubation with TGF-β stimulation
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Result:Did not reduce TGF-β-induced increases in CD44s, CD44v8, or CD44v10 mRNA levels in hnRNP M-knockdown A549 cells.
Chemical Information
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CAS No. 748785-70-8
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Molecular Weight 273.38
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Formula C13H11N3S2
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SMILES
CC1=NC(SCC2=NC3=C(S2)C=CC=C3)=NC=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Kamo M, et al. Discovery of anti-cell migration activity of an anti-HIV heterocyclic compound by identification of its binding protein hnRNP M. Bioorg Chem. 2021;107:104627. [Content Brief]
[2]. Kamo M, et al. Synthesis of the biotinylated anti-HIV compound BMMP and the target identification study. Bioorg Med Chem Lett. 2016;26(1):43-45. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)