2222-07-3 Usage
Definition
ChEBI: A cucurbitacin that is 9,10,14-trimethyl-4,9-cyclo-9,10-secocholesta-2,5,23-triene substituted by hydroxy groups at positions 2, 16, 20 and 25 and oxo groups at positions 1, 11 and 22.
Biological Activity
Selective inhibitor of STAT3/JAK2 signaling. Inhibits the activation of STAT3 and JAK2 and displays no activity on Src, Akt, ERK and JNK. Suppresses phosphotyrosine levels of STAT3, inhibits STAT3 DNA binding and STAT3-mediated gene expression. Induces apoptosis in cell lines expressing constitutively active tyrosine-phosphorylated STAT3.
Biochem/physiol Actions
Cucurbitacin I (JSI-124) is a novel selective inhibitor of the janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway with anti-proliferative and anti-tumor properties.
references
blaskovich ma, sun j, cantor a et al. discovery of jsi-124 (cucurbitacin i), a selective janus kinase/signal transducer and activator of transcription 3 signaling pathway inhibitor with potent antitumor activity against human and murine cancer cells in mice.cancer res. 2003 mar 15;63(6):1270-9.yu h, lee h, herrmann a et al. revisiting stat3 signalling in cancer: new and unexpected biological functions.nat rev cancer. 2014 nov;14(11):736-46. doi: 10.1038/nrc3818.song j, liu h, li z et al. cucurbitacin i inhibits cell migration and invasion and enhances chemosensitivity in colon cancer. oncol rep. 2015 apr;33(4):1867-71. qi j, xia g, huang cr et al. jsi-124 (cucurbitacin i) inhibits tumor angiogenesis of human breast cancer through reduction of stat3 phosphorylation. am j chin med. 2015;43(2):337-47.kim hj, kim jk et al. antiangiogenic effects of cucurbitacin-i. arch pharm res. 2015 feb;38(2):290-8. yuan g, yan sf, xue h et al. cucurbitacin i induces protective autophagy in glioblastoma in vitro and in vivo. j biol chem. 2014 apr 11;289(15):10607-19.
Check Digit Verification of cas no
The CAS Registry Mumber 2222-07-3 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 2,2,2 and 2 respectively; the second part has 2 digits, 0 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 2222-07:
(6*2)+(5*2)+(4*2)+(3*2)+(2*0)+(1*7)=43
43 % 10 = 3
So 2222-07-3 is a valid CAS Registry Number.
InChI:InChI=1/C30H42O7/c1-25(2,36)12-11-21(33)30(8,37)23-19(32)14-27(5)20-10-9-16-17(13-18(31)24(35)26(16,3)4)29(20,7)22(34)15-28(23,27)6/h9,11-13,17,19-20,23,31-32,36-37H,10,14-15H2,1-8H3/b12-11+
2222-07-3Relevant articles and documents
Cucurbitacin derivatives and preparation method thereof
-
Paragraph 0129, (2018/04/21)
The invention discloses multiple new derivatives of cucurbitacin-B and cucurbitacin-E and salts of the new derivatives, and also discloses a preparation method of the new derivatives. As the new derivatives and the salts thereof have the same basic structures as cucurbitacin-B and cucurbitacin-E respectively, the nature of the new derivatives and the salts thereof is basically the same as that ofcucurbitacin-B and cucurbitacin-E, and the new derivatives and the salts thereof have good anti-cancer, anti-virus, anti-inflammation and liver protection effects with low toxic and side effects.
Cucurbitacin E as a new inhibitor of cofilin phosphorylation in human leukemia U937 cells
Nakashima, Souichi,Matsuda, Hisashi,Kurume, Ai,Oda, Yoshimi,Nakamura, Seikou,Yamashita, Masayuki,Yoshikawa, Masayuki
experimental part, p. 2994 - 2997 (2010/08/20)
Cucurbitane-type triterpenes, cucurbitacins B and E, were reported to exhibit cytotoxic effects in several cell lines mediated by JAK/STAT3 signaling. However, neither compound inhibited phosphorylation of STAT3 in human leukemia (U937) cells at low concentrations. We therefore synthesized a biotin-linked cucurbitacin E to isolate target proteins based on affinity for the molecule. As a result, cofilin, which regulates the depolymerization of actin, was isolated and suggested to be a target. Cucurbitacins E and I inhibited the phosphorylation of cofilin in a concentration-dependent manner, and their effective concentrations having the same range as the concentrations at which they had cytotoxic effects in U937 cells. In addition, the fibrous-/globular-actin ratio was decreased after treatment with cucurbitacin E in HT1080 cells. These findings suggested that the inhibition of cofilin's phosphorylation increased the severing activity of cofilin, and then the depolymerization of actin was enhanced after treatment with cucurbitacin E at lower concentrations.
