PTC 209

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Cat.No. 5191 - PTC 209 | C17H13Br2N5OS | CAS No. 315704-66-6
Description: Bmi-1 inhibitor; antitumor
Chemical Name: N-(2,6-Dibromo-4-methoxyphenyl)-4-(2-methylimidazo[1,2-a]pyrimidin-3-yl)-2-thiazolamine
Purity: ≥98% (HPLC)
Datasheet
Citations
Literature

Biological Activity

Bmi-1 inhibitor (IC50 ~ 0.5 μM); irreversibly impairs colorectal cancer-initiating cell (CIC) growth. Reduces tumor growth in CIC xenograft assays and results in reduced potential of colorectal cancer cells to initiate tumors in vivo.

Technical Data

M. Wt 495.19
Formula C17H13Br2N5OS
Storage Store at -20°C
Purity ≥98% (HPLC)
CAS Number 315704-66-6
PubChem ID 1117196
InChI Key XVOOCQSWCCRVDY-UHFFFAOYSA-N
Smiles CC3=C(N(C=CC=N4)C4=N3)C1=CSC(NC2=C(Br)C=C(OC)C=C2Br)=N1

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

All Tocris products are intended for laboratory research use only.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
Solubility
DMSO 49.52 100
ethanol 9.9 20

Preparing Stock Solutions

The following data is based on the product molecular weight 495.19. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.

Select a batch to recalculate based on the batch molecular weight:
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 2.02 mL 10.1 mL 20.19 mL
5 mM 0.4 mL 2.02 mL 4.04 mL
10 mM 0.2 mL 1.01 mL 2.02 mL
50 mM 0.04 mL 0.2 mL 0.4 mL

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Product Datasheets

Safety Datasheet

References

References are publications that support the products' biological activity.

Kreso et al (2014) Self-renewal as a therapeutic target in human colorectal cancer. Nat.Med. 20 29 PMID: 24292392


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Literature in this Area

Programmed Cell Death

Programmed Cell Death Poster

There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.

Pathways for PTC 209

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