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CR-1-31-B

Catalog No. T38753 CAS 1352914-52-3

CR-1-31-B, a synthetic rocaglate, acts as a highly potent inhibitor of eIF4A. By disrupting the interaction between eIF4A and RNA, it effectively obstructs the initiation phase of protein synthesis. Specifically, CR-1-31-B interferes with the association between Plasmodium falciparum eIF4A (PfeIF4A) and RNA. Additionally, CR-1-31-B induces apoptosis in neuroblastoma and gallbladder cancer cells [4].

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CR-1-31-B, CAS 1352914-52-3

Pack Size	Availability	Price/USD
5 mg	Inquiry	$ 698.00
10 mg	Inquiry	$ 1,190.00
25 mg	Inquiry	$ 2,360.00

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Biological Description

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Description	CR-1-31-B, a synthetic rocaglate, acts as a highly potent inhibitor of eIF4A. By disrupting the interaction between eIF4A and RNA, it effectively obstructs the initiation phase of protein synthesis. Specifically, CR-1-31-B interferes with the association between Plasmodium falciparum eIF4A (PfeIF4A) and RNA. Additionally, CR-1-31-B induces apoptosis in neuroblastoma and gallbladder cancer cells [4].
In vitro	CR-1-31-B (100 nM; 24 hours) inhibits MUC1-C translation in MCF-10A cells (EGF-stimulated)[1]. CR-1-31-B (10 and 100 nM) decreases MUC1-C abundance in MDA-MB-468 breast cancer cells[1]. CR-1-31B sensitizes gallbladder cancer cells to TRAIL-mediated apoptosis through the translational downregulation of c-FLIP[2]. Neuroblastoma (NB) cell lines exhibit decreased viability, increased apoptosis rates as well as changes in cell cycle distribution when treated with the synthetic rocaglate CR-1-31-B (24-72 hours), which clamps eIF4A and eIF4F onto mRNA, resulting in a translational block[4]. CR-1-31-B (100 nM; 5 hours) treatment increases reverse glutamine metabolism in pancreatic cancer cells[5]. Western Blot Analysis[1]Cell Line: MCF-10A cells (EGF-stimulated) Concentration: 100 nM Incubation Time: 24 hours Result: Blocked increases in MUC1-C abundance. Cell Viability Assay[4]Cell Line: SH-SY5Y cells and Kelly cells Concentration: 0.1-100 nM Incubation Time: 24-72 hours Result: A significant decrease in SH-SY5Y viability was observed at 10 nM for all time points. Significantly decreased the viability of Kelly cells at 5 nM. The calculated IC 50 at 48 h was 20 nM for SH-SY5Y and 4 nM for Kelly cells. Apoptosis Analysis[4]Cell Line: SH-SY5Y and Kelly cells Concentration: SH-SY5Y cells were treated with 10, 20, and 50 nM and Kelly cells with 1, 5, and 10 nM Incubation Time: 24-72 hours Result: Triggered apoptosis.
In vivo	CR-1-31-B, administered intraperitoneally (IP) at a dosage of 2 mg/kg in 60 μL of olive oil once every two days over 28 days, effectively reduces growth and induces TRAIL-mediated apoptosis in gallbladder cancer cells (GBC) within a BALB/c nude mouse model[2]. Additionally, at a lower dosage of 0.2 mg/kg IP daily for 7 days in a murine orthotopic transplant model of pancreatic ductal adenocarcinoma, CR-1-31-B significantly inhibits protein synthesis and tumor growth in pancreatic cancers[5].

Molecular Weight	507.539
Formula	C28H29NO8
CAS No.	1352914-52-3

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

References and Literature

1. Jin C, Rajabi H, Rodrigo CM, Porco JA Jr, Kufe D. Targeting the eIF4A RNA helicase blocks translation of the MUC1-C oncoprotein. Oncogene. 2013;32(17):2179-2188. 2. Cao Y, et al. Targeting eIF4A using rocaglate CR 1 31B sensitizes gallbladder cancer cells to TRAIL mediated apoptosis through the translational downregulation of c FLIP. Oncol Rep. 2021;45(1):230-238. 3. Langlais D, et al. Rocaglates as dual-targeting agents for experimental cerebral malaria. Proc Natl Acad Sci U S A. 2018;115(10):E2366-E2375. 4. Skofler C, et al. Eukaryotic Translation Initiation Factor 4AI: A Potential Novel Target in Neuroblastoma. Cells. 2021;10(2):301. Published 2021 Feb 2. 5. Chan K, et al. eIF4A supports an oncogenic translation program in pancreatic ductal adenocarcinoma. Nat Commun. 2019;10(1):5151. Published 2019 Nov 13.

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Keywords

CR-1-31-B 1352914-52-3 CR 1 31 B CR131B inhibitor inhibit

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