Hydrocotarnine

• CAT Number: I042983
• CAS Number: 550-10-7
• Molecular Formula: C12H15NO3
• Molecular Weight: 221.25
• Purity: ≥95%
• Synonyms: 4-methoxy-6-methyl-7,8-dihydro-5H-[1,3]dioxolo[4,5-g]isoquinoline
• InChI: InChI=1S/C12H15NO3/c1-13-4-3-8-5-10-12(16-7-15-10)11(14-2)9(8)6-13/h5H,3-4,6-7H2,1-2H3
• InChIKey: XXANNZJIZQTCBP-UHFFFAOYSA-N
• SMILES: CN1CCC2=CC3=C(C(=C2C1)OC)OCO3

Hydrocotarnine is a Cbl inhibitor, and results in inflammasome-mediated IL-18 secretion in colitis. Hydrocotarnine increases expression of GLUT1 and cellular glucose uptake in glycolytic metabolism. Hydrocotarnine acts as an agent that provides analgesic effect in cancer research[1][2][3].
Hydrocotarnine is an analgesic agent (CRIN-2), with the patent ID of WO2011160016A2[1].
Hydrocotarnine (10 μM; 1 h) elevates the secretion of IL-1β and IL-18, and (0.1-10 μM; 1 h) increases the global level of tyrosine-phosphorylated proteins in THP-1 cells[1].
Hydrocotarnine (50 μM; 0-100 min) increases the glycolytic capacity and glycolytic reserve capacity in THP-1-derived macrophages[2].
Hydrocotarnine (50 μM; 16 h) inhibits Cbl and increases the total GLUT1 protein in THP-1-derived macrophages[2].
Hydrocotarnine is known to enhance the analgesic effect of opioids, and alleviates cancer pain[3].
Hydrocotarnine (10 mg/kg/d; i.p.; 9 d) shows inhibitory effect on Cbl and results in increasing IL-18 levels, indicating that NLRP3 inflammasome activation is enhanced in mice[1].
Hydrocotarnine (10 mg/kg/d; i.p.; 9 d) protects mice from DSS-induced colitis, with low scores of pathological evaluation of inflammation, epithelial defects, and crypt atrophy[1].

Reference

[1]. Chung IC, et al. Src-family kinase-Cbl axis negatively regulates NLRP3 inflammasome activation. Cell Death Dis. 2018 Oct 31;9(11):1109.
 [Content Brief]

[2]. Lin HC, et al. Cbl Negatively Regulates NLRP3 Inflammasome Activation through GLUT1-Dependent Glycolysis Inhibition. Int J Mol Sci. 2020 Jul 19;21(14):5104.
 [Content Brief]

[3]. Kim KU, et al. DITMD-induced mitotic defects and apoptosis in tumor cells by blocking the polo-box domain-dependent functions of polo-like kinase 1. Eur J Pharmacol. 2019 Mar 15;847:113-122.
 [Content Brief]