| Identification | Back Directory | [Name]
4-[(3R)-3-methylmorpholin-4-yl]-6-[(2R)-2-(trifluoro
methyl)piperidin-1-yl]-1,2-dihydropyridin-2-one | [CAS]
2126737-28-6 | [Synonyms]
4-[(3R)-3-methylmorpholin-4-yl]-6-[(2R)-2-(trifluoro
methyl)piperidin-1-yl]-1,2-dihydropyridin-2-one | [Molecular Formula]
C16H22F3N3O2 | [MDL Number]
MFCD32853054 | [MOL File]
2126737-28-6.mol | [Molecular Weight]
345.36 |
| Chemical Properties | Back Directory | [Boiling point ]
432.2±45.0 °C(Predicted) | [density ]
1.288±0.06 g/cm3(Predicted) | [solubility ]
Acetonitrile: Slightly soluble: 0.1-1 mg/ml
DMSO: Sparingly soluble: 1-10 mg/ml | [form ]
Solid | [pka]
10.99±0.10(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Description]
SB02024 is a VPS34 inhibitor. SB02024 activates cGAS-STING signaling and sensitizes tumors to STING agonist. SB02024 blocked autophagy in vitro and reduced xenograft growth of two breast cancer cell lines, MDA-MB-231 and MCF-7, in vivo. Vps34 inhibitor significantly potentiated cytotoxicity of Sunitinib and Erlotinib in MCF-7 and MDA-MB-231 in vitro in monolayer cultures and when grown as multicellular spheroids. Our data suggests that inhibition of autophagy significantly improves sensitivity to Sunitinib and Erlotinib and that Vps34 is a promising therapeutic target for combination strategies in breast cancer. | [Uses]
SB02024 is a potent and orally active VPS34 inhibitor. SB02024 inhibits Vps34 kinase activity. SB02024 induces CCL5 and CXCL10 via STAT1/IRF7. SB02024 shows anticancer activity[1][2][3]. | [in vivo]
SB02024 (20 mg/kg, Oral gavage) decreases the tumor growth and improves the effect benefit of anti-PD-L1/PD-1[1].
SB02024 increases the levels of CCL5 and CXCL10 in the blood plasma of B16-F10 and CT26 tumor-bearing mice, but dose not increase CCL5 or CXCL10 levels in the blood of non-tumor-bearing mice[1].
| Animal Model: | C57BL/6, BALB/C, immunodeficient NSG mice (7 weeks old)[1] | | Dosage: | 20 mg/kg | | Administration: | Oral gavage | | Result: | Decreased the tumor growth and weight of B16-F10 and CT26 and prolonged the survival of tumor-bearing mice. |
| [IC 50]
Vps34; STAT1 | [References]
[1] Noman MZ, et al. Inhibition of Vps34 reprograms cold into hot inflamed tumors and improves anti-PD-1/PD-L1 immunotherapy. Sci Adv. 2020 Apr 29;6(18):eaax7881. DOI:10.1126/sciadv.aax7881
[2] Yu Y, et al. Combining VPS34 inhibitors with STING agonists enhances type I interferon signaling and anti-tumor efficacy. Mol Oncol. 2024 Mar 20. DOI:10.1002/1878-0261.13619
[3] Bassam Claude JANJI, et al. Biomarker. Patent WO2020008046 A1. |
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