JPS016
Based on 1 publication(s) in Google Scholar
JPS016 is a class I histone deacetylase (HDAC) PROTAC inhibitor. JPS016 recruits the VHL E3 ligase (Ligands for E3 Ligase) to mediate the ubiquitination and proteasomal degradation of HDAC1, HDAC2 and HDAC3. JPS016 reduces the viability of colon cancer cells and induces Apoptosis. JPS016 activates the PINK1/Parkin mitochondrial Autophagy pathway, enhances cardiomyocyte viability, alleviates mitochondrial damage, and reduces mitochondrial ROS production in cells. JPS016 is applicable to research related to colon cancer and sepsis cardiomyopathy.
(Pink: HDAC ligand (HY-50934); Blue: VHL ligand (HY-125845); Black: linker (HY-175977)).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2669785-77-5
- Formel: C48H63N7O8S
- Molecular Weight:898.12
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) JPS016
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Biologische Aktivität
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VHL |
HDAC1 |
HDAC2 |
HDAC3 |
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Cell Line
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Type | Value | Description | References |
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| HCT-116 | EC50 |
5.2 μM
Compound: 9; JPS016
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Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability measured after 48 hrs by cell-titer glo assay
Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability measured after 48 hrs by cell-titer glo assay
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[PMID: 35293758] |
JPS016 (Compound 9) (0.001-100 μM; 24 h) potently degrades HDAC1 (DC50 = 0.55 μM, Dmax = 77%) and HDAC3 (DC50 = 0.53 ± 0.13 μM, Dmax = 66%) in HCT116 cells after 24 h of treatment[1].
JPS016 (10 μM; 2-48 h) upregulates the acetylation level of histone H3K56 in HCT116 cells in a time-dependent manner in vitro, with the acetylation peak occurring at 36 h[1].
JPS016 (1-10 μM; 24-48 h) reduces the stability of LSD1 and SIN3A, components of the HDAC1/2 corepressor complex, in HCT116 cells[1].
JPS016 (0.1-100 μM; 48 h) reduces the viability of HCT116 cells, with an EC50 of 5.3 μM after 48 h of treatment[1].
JPS016 (10 μM; 24-48 h) induces apoptosis in HCT116 cells. After 48 h of treatment, 70% of cells are present in the apoptotic sub-G1 population, and the drug significantly enriches genes related to cell cycle arrest and apoptosis[1].
JPS016 (24 h) protects HL-1 mouse cardiomyocytes against LPS (HY-D1056)-induced injury by restoring cell viability and reducing cytotoxicity, and decreases LPS-induced mitochondrial ROS production in cells[2].
JPS016 (0.01-10 μM) induces dose-dependent degradation of class I HDACs in both untreated and LPS-stimulated HL-1 mouse cardiomyocytes, with preferential activity against HDAC1, HDAC3 and HDAC8[2].
JPS016 (24 h) enhances histone acetylation and lactylation modifications in HL-1 mouse cardiomyocytes. Specifically, under LPS-induced SCM stress conditions, it reverses the LPS-induced pathogenic gene program, regulates mitochondria-related cellular processes in HL-1 mouse cardiomyocytes, and promotes exosome formation and mitochondrial extrusion in HL-1 mouse cardiomyocytes under LPS-induced SCM stress[2].
JPS016 (administered for 24 h) activates the PINK1/Parkin mitophagy pathway in HL-1 mouse cardiomyocytes under LPS-induced SCM stress[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT116 human colon carcinoma cells
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Concentration:0.01-10 μM (24 h dose-response); 10 μM (time-course)
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Incubation Time:2-48 h (time-course); 24 h (dose-response)
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Result:Reduced HDAC1 to 25%, HDAC2 to 50%, HDAC3 to 50% at 0.1 μM for 24 h.
Reduced HDAC1 to 25%, HDAC2 to 75%, HDAC3 to 25% at 1 μM for 24 h.
Reduced HDAC1 to 25%, HDAC2 to 75%, HDAC3 to ~100% (hook effect) at 10 μM for 24 h.
Reached 84% degradation of HDAC1 and 51% degradation of HDAC2 by 48 h at 10 μM.
Reached ~50% degradation of HDAC3 at 36 and 48 h at 10 μM.
Showed DC50 values of 0.55 ± 0.18 μM (HDAC1) and 0.53 ± 0.13 μM (HDAC3), with Dmax values of 77% (HDAC1), 45% (HDAC2), 66% (HDAC3) after 24 h dose-response testing.
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Cell Line:HCT116 human colon carcinoma cells
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Concentration:1, 10 μM
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Incubation Time:24-48 h
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Result:Reduced SIN3A levels to 60% of controls at 10 μM for 24 h.
Reduced LSD1 levels significantly to approximately 40% of controls at 10 μM for 48 h.
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Cell Line:HCT116 human colon carcinoma cells
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Concentration:0.1-100 μM
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Incubation Time:48 h
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Result:Showed an EC50 value of 5.3 μM for reducing cell viability.
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Cell Line:HCT116 human colon carcinoma cells
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Concentration:10 μM
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Incubation Time:2, 4, 8, 15, 24, 36, 48 h
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Result:Increased H3K56ac by 2-fold after 8 h compared to DMSO control.
Reached maximum fold change after 36 h, then slightly decreased at 48 h.
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Cell Line:HCT116 human colon carcinoma cells
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Concentration:10 μM
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Incubation Time:24, 48 h
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Result:Induced 30% of cells in apoptotic sub-G1 population at 24 h.
Induced 70% of cells in apoptotic sub-G1 population at 48 h.
Chemical Information
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CAS. Nr. 2669785-77-5
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Molecular Weight 898.12
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Formel C48H63N7O8S
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SMILES
O=C(N(C[C@@H]1O)[C@@H](C1)C(NCC2=CC=C(C(SC=N3)=C3C)C=C2)=O)[C@H](C(C)(C)C)NC(COCCCCCCCCCOCC(NC(C=C4)=CC=C4C(NC(C=CC=C5)=C5N)=O)=O)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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Int J Biochem Cell Biol
PROTAC-mediated degradation of Class I HDACs by JPS016 alleviates septic cardiomyopathy via mitophagy-driven exopher formation and mitochondrial quality control. [Abstract]2026 Mar:192:106910. PMID: 41687730
Reinheit & Dokumentation
Verweise
[1]. Smalley JP, et al. Optimization of Class I Histone Deacetylase PROTACs Reveals that HDAC1/2 Degradation is Critical to Induce Apoptosis and Cell Arrest in Cancer Cells. J Med Chem. 2022 Apr 14;65(7):5642-5659. [Content Brief]
[2]. Li Z, et al. PROTAC-mediated degradation of Class I HDACs by JPS016 alleviates septic cardiomyopathy via mitophagy-driven exopher formation and mitochondrial quality control. Int J Biochem Cell Biol. 2026;192:106910. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
JPS016 Related Classifications
HY-145816 Related Classifications
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