This is a demo store. No orders will be fulfilled.

cRIPGBM chloride - 99%, high purity , CAS No.2361988-77-2

    Grade & Purity:
  • ≥99%
In stock
Item Number
C650756
Grouped product items
SKU Size
Availability
Price Qty
C650756-5mg
5mg
Available within 8-12 weeks(?)
Production requires sourcing of materials. We appreciate your patience and understanding.
$80.90
C650756-10mg
10mg
Available within 8-12 weeks(?)
Production requires sourcing of materials. We appreciate your patience and understanding.
$130.90
C650756-25mg
25mg
Available within 8-12 weeks(?)
Production requires sourcing of materials. We appreciate your patience and understanding.
$270.90
C650756-50mg
50mg
Available within 8-12 weeks(?)
Production requires sourcing of materials. We appreciate your patience and understanding.
$430.90
C650756-100mg
100mg
Available within 8-12 weeks(?)
Production requires sourcing of materials. We appreciate your patience and understanding.
$680.90

Basic Description

Specifications & Purity ≥99%
Biochemical and Physiological Mechanisms cRIPGBM chloride, an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1 -dependent ap
Storage Temp Store at 2-8°C,Desiccated
Shipped In
Wet ice
This product requires cold chain shipping. Ground and other economy services are not available.
Product Description

cRIPGBM chloride, an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1 -dependent apoptosis . cRIPGBM(chloride) suppresses the formation of RIPK2/TAK1 (prosurvival complex), and increases the formation of RIPK2/caspase 1 (proapoptotic complex). cRIPGBM(chloride) exerts potent anti-tumor activity in vivo in animal models

In Vitro

cRIPGBM chloride (0.25 μM; 0-24 h) time-dependently activates caspase 1, caspase 9, and caspase 7, as well as PARP cleavage, in CBM-1 GBM CSCs. cRIPGBM chloride (0.125 μM, 0.25 μM; 24 h) induces cell apoptosis mediated by caspase 1 in CBM-1 GBM CSCs. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: GBM-1 GBM CSCs Concentration: 50 nM, 100 nM, 125 nM, 250 nM, and 500 nM Incubation Time: 3 h, 6 h, 12 h, and 24 h Result: Had the ability to regulate RIPK2 to act as a prosurvival or proapoptotic molecule. Significantly reduced RIPK2 binding to cIAP2 in a dose-dependent manner.

In Vivo

cRIPGBM chloride (50 mg/kg; p.o.; twice daily for 5 weeks) inhibits tumor growth in patient-derived GBM CSC intracranial xenograft mouse models . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Orthotopic intracranial xenograft model in mouse Dosage: 50 mg/kg Administration: PO; twice daily, 8 h apart, starting at day 7 postinjection; last for 5 weeks Result: Monitored by Fluorescence Tomography System. Decreased the tumor signal, as well as tumor size.

Form:Solid

IC50& Target:Caspase-1 RIPK2

Names and Identifiers

IUPAC Name 3-benzyl-1-[(4-fluorophenyl)methyl]-2-methylbenzo[f]benzimidazol-3-ium-4,9-dione;chloride
INCHI InChI=1S/C26H20FN2O2.ClH/c1-17-28(15-18-7-3-2-4-8-18)23-24(29(17)16-19-11-13-20(27)14-12-19)26(31)22-10-6-5-9-21(22)25(23)30;/h2-14H,15-16H2,1H3;1H/q+1;/p-1
InChIKey IHNGETPFBJHWFE-UHFFFAOYSA-M
Smiles CC1=[N+](C2=C(N1CC3=CC=C(C=C3)F)C(=O)C4=CC=CC=C4C2=O)CC5=CC=CC=C5.[Cl-]
PubChem CID 156024495
Molecular Weight 446.90

Certificates(CoA,COO,BSE/TSE and Analysis Chart)

C of A & Other Certificates(BSE/TSE, COO):
Analytical Chart:

Chemical and Physical Properties

Solubility DMSO : 25 mg/mL (55.94 mM; ultrasonic and warming and heat to 60°C)

Solution Calculators

Reviews

Customer Reviews

Shall we send you a message when we have discounts available?

Remind me later

Thank you! Please check your email inbox to confirm.

Oops! Notifications are disabled.