CPTH2 hydrochloride
Based on 2 publication(s) in Google Scholar
CPTH2 hydrochloride is a potent histone acetyltransferase (HAT) inhibitor. CPTH2 hydrochloride selectively inhibits the acetylation of histone H3 by Gcn5. CPTH2 hydrochloride induces apoptosis and decreases the invasiveness of a clear cell renal carcinoma (ccRCC) cell line through the inhibition of acetyltransferase p300 (KAT3B).
For research use only. We do not sell to patients.
- CAS No.: 2108899-91-6
- Formula: C14H15Cl2N3S
- Molecular Weight:328.26
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) CPTH2 hydrochloride
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Biological Activity
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GCN5 |
CPTH2 (100 μM; 12, 24, 48 hours) hydrochloride causes a decrease in cell proliferation after as early as 12 h with a further significant reduction after 48 h stimulation[1].
CPTH2 (100 μM; 12 or 48 hours) hydrochloride causes a comparable drop of the activity in both cell lines[1].
CPTH2 (100 μM; 48 hours) hydrochloride produces a drastic increase in apoptotic/dead cell population after 48 h[1].
CPTH2 (100 μM; 12, 24, 48 hours) hydrochloride shows a reduced acetylation of both global AcH3 histone and H3AcK18[1].
CPTH2 (100 μM; 24, 48 hours) hydrochloride is capable to counteract invasion and migration of ccRCC-786-O cells in culture[1].
CPTH2 (0.2, 0.5, 1 mM) hydrochloride inhibits the growth of a GCN5 deleted strain and a single catalytic mutant E173H[2].
CPTH2 (0.6, 0.8 mM; for 24 hours) hydrochloride inhibits histone H3 acetylation in yeast cell cultures[2].
CPTH2 hydrochloride inhibits the Gcn5p dependent functional network[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Papillary thyroid (K1) and clear cell Renal Cell Carcinoma (ccRCC-786-O) cell lines
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Concentration:100 μM
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Incubation Time:12, 24, 48 hours
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Result:Caused a decrease in cell proliferation after as early as 12 h with a further significant reduction after 48 h stimulation.
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Cell Line:K1 and ccRCC-786-O cell lines
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Concentration:100 μM
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Incubation Time:24 hours (K1 cell) and 48 hours (ccRCC-786-O cell)
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Result:Caused a comparable drop of the activity in both cell lines.
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Cell Line:ccRCC-786-O cells
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Concentration:100 μM
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Incubation Time:48 hours
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Result:Produced a drastic increase in apoptotic/dead cell population after 48 h.
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Cell Line:ccRCC-786-O cells
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Concentration:100 μM
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Incubation Time:12, 24, 48 hours
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Result:Showed a reduced acetylation of both global AcH3 histone and H3AcK18.
Chemical Information
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CAS No. 2108899-91-6
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Molecular Weight 328.26
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Formula C14H15Cl2N3S
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SMILES
ClC1=CC=C(C2=CSC(N/N=C3CCCC/3)=N2)C=C1.[H]Cl
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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.
Publications (2)
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Journal Impact Factor
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Most Recent
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Immunity
Palmitic acid reprograms neutrophils to compromise vascular integrity and promote breast cancer lung metastasis. [Abstract]2026 Jul 14;59(7):1964-1981.e9. PMID: 42034064 -
Purity & Documentation
References
[1]. Cocco E, et al. KAT3B-p300 and H3AcK18/H3AcK14 levels are prognostic markers for kidney ccRCC tumoraggressiveness and target of KAT inhibitor CPTH2. Clin Epigenetics. 2018 Apr 4;10:44. [Content Brief]
[2]. Chimenti F, et al. A novel histone acetyltransferase inhibitor modulating Gcn5 network: cyclopentylidene-[4-(4'-chlorophenyl)thiazol-2-yl)hydrazone. J Med Chem. 2009 Jan 22;52(2):530-6. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)