GBD-9 is a double-mechanism efficient degrader of BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). GBD-9 acts both as a PROTAC molecule to induce the degradation of BTK and as a molecular glue to degrade GSPT1.It exhibits anti-proliferative effects, inhibiting cancer cell survival.

GBD-9 is a double-mechanism efficient degrader of BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). GBD-9 acts both as a PROTAC molecule to induce the degradation of BTK and as a molecular glue to degrade GSPT1.It exhibits anti-proliferative effects, inhibiting cancer cell survival.

GBD-9 is a double-mechanism efficient degrader of BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). GBD-9 acts both as a PROTAC molecule to induce the degradation of BTK and as a molecular glue to degrade GSPT1.It exhibits anti-proliferative effects, inhibiting cancer cell survival.

GBD-9 is a double-mechanism efficient degrader of BTK and GSPT1 by recruiting the E3 ligase cereblon (CRBN). GBD-9 acts both as a PROTAC molecule to induce the degradation of BTK and as a molecular glue to degrade GSPT1.It exhibits anti-proliferative effects, inhibiting cancer cell survival.

TL13-112 is a degrader of anaplastic lymphoma kinase (ALK) with an IC50 of 0.60 nM. It demonstrates anti-proliferative activity in non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphoma (ALCL) cell lines.

TL13-112 is a degrader of anaplastic lymphoma kinase (ALK) with an IC50 of 0.60 nM. It demonstrates anti-proliferative activity in non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphoma (ALCL) cell lines.

TL13-112 is a degrader of anaplastic lymphoma kinase (ALK) with an IC50 of 0.60 nM. It demonstrates anti-proliferative activity in non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphoma (ALCL) cell lines.

TL13-112 is a degrader of anaplastic lymphoma kinase (ALK) with an IC50 of 0.60 nM. It demonstrates anti-proliferative activity in non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphoma (ALCL) cell lines.

Fulzerasib (IBI351, GFH925) is an irreversible small molecule inhibitor for KRAS G12C mutation blocking KRAS pathway signaling pERK with an IC50 of 37 nM. It demonstrates potent anti-tumor activity in multiple KRAS G12C-mutant tumor models including human pancreatic cancer, human lung adenocarcinoma, colorectal adenocarcinoma, and lung cancer models.

Fulzerasib (IBI351, GFH925) is an irreversible small molecule inhibitor for KRAS G12C mutation blocking KRAS pathway signaling pERK with an IC50 of 37 nM. It demonstrates potent anti-tumor activity in multiple KRAS G12C-mutant tumor models including human pancreatic cancer, human lung adenocarcinoma, colorectal adenocarcinoma, and lung cancer models.