98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

GGTI 298 TFA salt；
GGTI 298 (trifluoroacetate salt)

solid

DMSO ：100 mg/mL (168.44 mM)

Ethanol ：100 mg/mL (168.44 mM)

Rap1A

RhoA inhibitor (GGTI298 Trifluoroacetate) significantly reduces cAMP agonist-stimulated apical K+ conductance. Knockdown of DR4 abolishes NF-κB activation, leading to sensitization of DR5-dependent apoptosis induced by the combination of GGTI298 Trifluoroacetate and TRAIL. GGTI298 Trifluoroacetate/TRAIL activates NF-κB and inhibits Akt. Knockdown of DR5, prevents GGTI298/TRAIL-induced IκBα and p-Akt reduction, suggesting that DR5 mediates reduction of IκBα and p-Akt induced by GGTI298/TRAIL. In contrast, DR4 knockdown further facilitates GGTI298/TRAIL-induced p-Akt reduction.

The vivo mouse ileal loop experiments show fluid accumulation is reduced in a dose-dependent manner by TRAM-34, GGTI298 Trifluoroacetate, or H1152 when inject together with cholera toxin into the loop.

1.Li, X.,Liu, L.,Tupper, J.C., et al. Inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathway induces apoptosis in human endothelial cells. The Journal of Biological Chemisty 277(18), 15309-15316 (2002).

2.Miquel, K.,Pradines, A.,Sun, J., et al. GGTI-298 induces G₀-G₁ block and apoptosis whereas FTI-277 causes G₂-M enrichment in A549 cells. Cancer Research 57, 1846-1850 (1997).

3.Efuet, E.T. and Keyomarsi, K. Farnesyl and geranylgeranyl transferase inhibitors induce G₁ arrest by targeting the proteasome. Cancer Research 66(2), 1040-1051 (2006).

4.Vogt, A.,Sun, J.,Qian, Y., et al. The geranylgeranyltransferase-I inhibitor GGTI-298 arrests human tumor cells in G₀/G₁ and induces p21WAF1/CIP1/SDI1 in a p53-independent manner. The Journal of Biological Chemisty 272(43), 27224-27229 (1997).