Top Suppliers:I want be here
Related CAS#:
2222-07-3 50298-90-3
58546-34-2 1110-02-7
77704-34-8 65247-27-0
5988-76-1 751-95-1
99530-82-2 3877-86-9
1158522-08-7 940364-43-2
134104-43-1 131615-57-1
6906-52-1 930439-75-1
40816-73-7 1018584-77-4
1375289-11-4 849349-65-1

2222-07-3

2222-07-3 structure
2222-07-3 structure
  • Name: Cucurbitacin I
  • Chemical Name: cucurbitacin I
  • CAS Number: 2222-07-3
  • Molecular Formula: C30H42O7
  • Molecular Weight: 514.650
  • Catalog: Biochemical Plant extracts
  • Create Date: 2018-03-13 08:00:00
  • Modify Date: 2024-01-02 18:18:58
  • Cucurbitacin I is a natural selective inhibitor of JAK2/STAT3, with potent anti-cancer activity.
Name cucurbitacin I
Synonyms 2,16,20,26-Tetrahydroxy-9,10,14-trimethyl-4,9-cyclo-9,10-secocholesta-2,5,24-triene-1,11,23-trione
CUCURBITACIN I
Estra-1,5-diene-3,11-dione, 17-(1,6-dihydroxy-1,5-dimethyl-3-oxo-4-hexen-1-yl)-2,16-dihydroxy-4,4,9,14-tetramethyl-
Description Cucurbitacin I is a natural selective inhibitor of JAK2/STAT3, with potent anti-cancer activity.
Related Catalog
Target

JAK2

STAT3

In Vitro Exposure of the COLO205 cells to Cucurbitacin I significantly decreases cell viability. The anticancer activity of Cucurbitacin I is accomplished by downregulating p-STAT3 and MMP-9 expression[1]. PE-induced cell enlargement and upregulation of ANF and β-MHC are significantly suppressed by pretreatment of the cardiomyocytes with Cucurbitacin I. Notably, Cucurbitacin I also impaires connective tissue growth factor (CTGF) and MAPK signaling, pro-hypertrophic factors, as well as TGF-β/Smad signaling, the important contributing factors to fibrosis[2]. Incubation of the Seax cell line with the Jak/Stat3 inhibitor Cucurbitacin I result in a time- and concentration-dependent decrease of P-Stat3 and Stat3. In freshly isolated Sz cells (n=3), Cucurbitacin I induces a concentration-dependent decrease in Stat3 expression whereas P-Stat3 is undetectable. Finally, incubation of freshly isolated Sz cells (n=4) with 30 μM Cucurbitacin I for 6 hours induces apoptosis in the large majority (73-91%) of tumor cells[3].
In Vivo No major side effects are noted throughout the study. It is shown that average tumor volumes at the end of the study are as follows: control, 616 mm3 (±130); CQ, 580 mm3 (±107); Cucurbitacin I, 346mm3 (±79); and combination, 220mm3 (±62). The differences in tumor volume between the Cucurbitacin I and control, combination and control, and combination and Cucurbitacin I arms are significant. Furthermore, combination-treated tumors exhibit a significantly lower average tumor weight at study termination than the control. Moreover, there was no effect on the body weights of mice[4].
Animal Admin Mice[4] BALB/c nude (nu/nu) female mice are used. U251 cells (5×106 cells in 50 μL of serum-free DMEM) are inoculated subcutaneously into the right flank of 5-week-old female mice after acclimatization for a week. Tumor growth is measured daily with calipers. When the tumors reach a mean volume of 90-120 mm3, animals are randomized into groups. In the first experiment, 16 mice are randomly assigned to Cucurbitacin I (1 mg/kg/day in 20% DMSO in PBS) or drug vehicle control (20% DMSO in PBS) and dosed intraperitoneally with 100 μL of vehicle or drug once daily for 18 days, whereas, in the second, 20 mice are assigned to four groups. Control animals receive 20% DMSO in PBS vehicle, whereas treated animals are injected with Cucurbitacin I (1 mg/kg/day) in 20% DMSO in PBS, CQ (25 mg/kg/day) in 20% DMSO in PBS, and Cucurbitacin I (1 mg/kg/day) plus CQ (25 mg/kg/day) in 20% DMSO in PBS and dosed intraperitoneally with 100 μL of vehicle or drug once daily for 15 days[4].
References

[1]. Song J, et al. Cucurbitacin I inhibits cell migration and invasion and enhances chemosensitivity in colon cancer. Oncol Rep. 2015 Apr;33(4):1867-71.

[2]. Jeong MH, et al. Cucurbitacin I Attenuates Cardiomyocyte Hypertrophy via Inhibition of Connective Tissue Growth Factor (CCN2) and TGF- β/Smads Signalings. PLoS One. 2015 Aug 21;10(8):e0136236.

[3]. van Kester MS, et al. Cucurbitacin I inhibits Stat3 and induces apoptosis in Sézary cells. J Invest Dermatol. 2008 Jul;128(7):1691-5.

[4]. Yuan G, et al. Cucurbitacin I induces protective autophagy in glioblastoma in vitro and in vivo. J Biol Chem. 2014 Apr 11;289(15):10607-19.
Density 1.3±0.1 g/cm3
Boiling Point 716.9±60.0 °C at 760 mmHg
Melting Point 148-150ºC
Molecular Formula C30H42O7
Molecular Weight 514.650
Flash Point 401.3±29.4 °C
Exact Mass 514.293030
PSA 132.13000
LogP 2.06
Vapour Pressure 0.0±5.2 mmHg at 25°C
Index of Refraction 1.594
Storage condition −20°C

CHEMICAL IDENTIFICATION

RTECS NUMBER :
RC6200000
CHEMICAL NAME :
19-Nor-9-beta,10-alpha-lanosta-1,5,23-triene-3,11,22- trione, 9-methyl-2,16,20,25- tetrahydroxy-
CAS REGISTRY NUMBER :
2222-07-3
LAST UPDATED :
199007
DATA ITEMS CITED :
1
MOLECULAR FORMULA :
C30-H42-O7
MOLECULAR WEIGHT :
514.72
WISWESSER LINE NOTATION :
L E5 B666 CV OV LU PUTJ B1 E1 FXQ1&V1U1XQ1&1 GQ I1 N1 N1 PQ

HEALTH HAZARD DATA

ACUTE TOXICITY DATA

TYPE OF TEST :
LD50 - Lethal dose, 50 percent kill
ROUTE OF EXPOSURE :
Oral
SPECIES OBSERVED :
Rodent - mouse
DOSE/DURATION :
5 mg/kg
TOXIC EFFECTS :
Details of toxic effects not reported other than lethal dose value
REFERENCE :
CHTPBA Chimica Therapeutica. (Paris, France) V.1-8, 1965-73. For publisher information, see EJMCA5. Volume(issue)/page/year: 4,459,1969
Hazard Codes T+:Verytoxic;
Risk Phrases R28
Safety Phrases S28-S36/37-S45
RIDADR UN 2811
RTECS RC6200000
Precursor  1

DownStream  0


Chemsrc provides CAS#:2222-07-3 MSDS, density, melting point, boiling point, structure, formula, molecular weight, synthetic route, etc.
title: CAS No. 2222-07-3 | Chemsrc address: https://www.chemsrc.com/en/baike/946829.html

Home | MSDS/SDS Database Search | Journals | Product Classification | Biologically Active Compounds | Selling Leads | About Us | Disclaimer

Copyright © 2024 ChemSrc All Rights Reserved