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MGH-CP1

Cat. No. M21662
MGH-CP1 Structure
Size Price Availability Quantity
5mg USD 68  USD68 In stock
10mg USD 105  USD105 In stock
25mg USD 230  USD230 In stock
50mg USD 400  USD400 In stock
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Quality Control & Documentation
Biological Activity

MGH-CP1 is a potent and orally active TEAD2 and TEAD4 auto-palmitoylation inhibitor with IC50s of 710 nM and 672 nM, respectively. MGH-CP1 can decrease the palmitoylation levels of endogenous or ectopically expressed TEAD proteins in cells. MGH-CP1 can suppress Myc expression, inhibit epithelial over-proliferation, and induce apoptosis when together with Lats1/2 deletion. MGH-CP1 potently inhibits TEAD-mediated transcription in a dose-dependent manner and effectively blocks cell over-proliferation.

In vivo, MGH-CP1 (75mg/kg; PO; daily, for 2 weeks) inhibits the palmitoylation of TEAD proteins in the intestinal epithelium in wild-type mice, but inhibits upregulation of the TEAD target genes, CTGF and ANKRD1, in Lats1/2 KO mice intestine.

Chemical Information
Molecular Weight 368.50
Formula C20H24N4OS
CAS Number 896657-58-2
Solubility (25°C) DMSO 80 mg/mL
Storage 2-8°C, protect from light, dry, sealed
Conversion of different model animals based on BSA (PMID: 27057123)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

References

[1] Yang Sun, et al. Nat Commun. Pharmacological blockade of TEAD-YAP reveals its therapeutic limitation in cancer cells

[2] Qi Li, et al. Cell Stem Cell. Lats1/2 Sustain Intestinal Stem Cells and Wnt Activation through TEAD-Dependent and Independent Transcription

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Keywords: MGH-CP1 supplier, Apoptosis, inhibitors, activators


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