For research use only. Not Intended for Therapeutic Use!
|IC50:||3.2 nM |
|We match the lowest price on market.|
TAK-733 is a potent and selective MEK allosteric site inhibitor for MEK1 with IC50 of 3.2 nM, inactive to Abl1, AKT3, c-RAF, CamK1, CDK2, c-Met, etc.
IC50 Value: 3.2 nM 
in vitro: Sensitivity of cutaneous and uveal melanoma cell lines to TAK733 was investigated. five cutaneous melanoma cell lines wild type for mutations in NRAS, BRAF, GNAQand GNA11 and only one was highly sensitive to TAK733 with IC50s below 1 nM, while two were considered sensitive with IC50 less than 10 nM. All five uveal melanoma cell lines were sensitive to TAK733 with IC50 values below 10 nM, with three of them being highly sensitive. All these cell lines carried GNAQ or GNA11 driver mutations. Inhibition of oncogenic MAPK signaling through MEK1 and MEK2 by TAK733 results in antitumor activity in vitro against a large subset of melanoma cell lines.
in vivo: The in vivo antitumor activity of TAK-733, an investigational potent, selective, non-ATP-competitive allosteric inhibitor of MEK, in combination with alisertib, an investigational potent, selective, reversible, ATP-competitive inhibitor of Aurora A kinase, was examined in experimental human solid tumor xenograft models including NSCLC (NCI H23 [KRAS and LKB1 mutations]), CRC (SW620 [KRAS, APC, p53 mutations]), and pancreatic cancer (Panc 1 and Capan 1 [KRAS mutations] and BxPC-3 [No MAPK mutations]) models in immunocompromised mice.
Clinical trail: TAK733 clinical trail I is on the way for cancer(Melanoma, NSCLC, colorectal, breast cancer .