Data from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Data from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Data from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Figure S2 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S2 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S3 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S4 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S4 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S5 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S5 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Figure S6 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Supplemental Text from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Supplemental Text from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Supplemental Text from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Supplementary Appendix S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Appendix S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Appendix S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Figure S2 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Figure S2 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Figure S2 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Figures from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Supplementary References from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary References from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations

Supplementary Table S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S2 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S2 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S3 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S3 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations

Supplementary Table S4 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S4 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S5 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S5 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Table S5 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Video 2 from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Supplementary Video 4 from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Supplementary Video 5 from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Supplementary Video 7 from Exploiting Allosteric Properties of RAF and MEK Inhibitors to Target Therapy-Resistant Tumors Driven by Oncogenic BRAF Signaling

Supplementary Video S1 Legend from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Video S1 Legend from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Video S1 Legend from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations

Supplementary Video S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Video S1 from RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across <i>FGFR2</i> Alterations and Resistance Mutations

Supplementary Video S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations

Table S1 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Table S1 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Table S1 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Table S2 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia

Table S3 from Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia