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Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo. Pharmacological targeting of CDs promotes response to KRASG12C inhibition.

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Presentation on theme: "Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo. Pharmacological targeting of CDs promotes response to KRASG12C inhibition."— Presentation transcript:

1 Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo.
Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo. (A) Tumor volumes in mice bearing H358 xenografts and treated with vehicle, ARS-1620 (100 mg/kg), erlotinib (80 to 100 mg/kg, EGFRi), or their combination. Treatment was stopped 54 days after initial implantation to monitor the durability of observed responses. n ≥ 4 mice per group; error bars denote SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < comparing ARS-1620 and combination arms by a Mann-Whitney test. (B) Tumor volumes in mice bearing MIA PaCa-2 xenografts and treated with vehicle, ARS-1620 (100 mg/kg), palbociclib (100 mg/kg, CDK4/6i), or their combination. n ≥ 8 mice per group; error bars denote SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < comparing ARS-1620 and combination arms by a Mann-Whitney test. Kevin Lou et al., Sci. Signal. 2019;12:eaaw9450 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works


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