James Watters
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View article: Supplementary Figure S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Figure S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Supplementary Figure 1. RLY-4008 is an irreversible inhibitor of FGFR2.
View article: Supplementary Table S3 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S3 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Antiproliferative effect of RLY-4008 and pan-FGFRi in human tumor cell lines
View article: Supplementary Table S5 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S5 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Fold change in potency against FGFR2 acquired resistance mutations
View article: Supplementary Table S4 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 FGFR2 alterations and resistance mutations Open
In vivo exposures of pan-FGFRi in mouse studies
View article: Supplementary References from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary References from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
three references cited in supplementary data
View article: Supplementary Appendix S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Appendix S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
ReFocus entry criteria
View article: Supplementary Video S1 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 FGFR2 alterations and resistance mutations Open
In this schematic movie, apo FGFR1 (left panel) demonstrates rapid P-loop dynamics, while apo FGFR2 (right panel) displays less P-loop motion.
View article: Supplementary Video S1 Legend from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 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 Open
Supplementary video legend describing schematic video of P-loop dynamics
View article: Supplementary Appendix S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Appendix S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
ReFocus entry criteria
View article: Supplementary Video S1 Legend from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 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 Open
Supplementary video legend describing schematic video of P-loop dynamics
View article: Supplementary Video S1 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 FGFR2 alterations and resistance mutations Open
In this schematic movie, apo FGFR1 (left panel) demonstrates rapid P-loop dynamics, while apo FGFR2 (right panel) displays less P-loop motion.
View article: Supplementary Table S4 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 FGFR2 alterations and resistance mutations Open
In vivo exposures of pan-FGFRi in mouse studies
View article: Supplementary Table S1 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 FGFR2 alterations and resistance mutations Open
Potency (kinact/KI) of RLY-4008 against FGFR1 and FGFR2
View article: Supplementary Table S3 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S3 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Antiproliferative effect of RLY-4008 and pan-FGFRi in human tumor cell lines
View article: Supplementary References from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary References from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
three references cited in supplementary data
View article: Supplementary Table S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Biochemical inhibition of FGFR by RLY-4008 and pan-FGFRi
View article: Supplementary Table S1 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 FGFR2 alterations and resistance mutations Open
Potency (kinact/KI) of RLY-4008 against FGFR1 and FGFR2
View article: Supplementary Figure S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Figure S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Supplementary Figure 2. Treatment with RLY-4008 is well-tolerated and leads to dose-dependent inhibition of FGFR2 and tumor regression in multiple FGFR2-altered tumor models.
View article: Supplementary Figure S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Figure S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Supplementary Figure 2. Treatment with RLY-4008 is well-tolerated and leads to dose-dependent inhibition of FGFR2 and tumor regression in multiple FGFR2-altered tumor models.
View article: Supplementary Table S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S2 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Biochemical inhibition of FGFR by RLY-4008 and pan-FGFRi
View article: Supplementary Table S5 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Table S5 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Fold change in potency against FGFR2 acquired resistance mutations
View article: Supplementary Figure S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Supplementary Figure S1 from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Supplementary Figure 1. RLY-4008 is an irreversible inhibitor of FGFR2.
View article: Data from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations
Data from RLY-4008, the first highly selective FGFR2 inhibitor with activity across FGFR2 alterations and resistance mutations Open
Oncogenic activation of fibroblast growth factor receptor 2 (FGFR2) drives multiple cancers and represents a broad therapeutic opportunity, yet selective targeting of FGFR2 has not been achieved. While the clinical efficacy of pan-FGFR inh…
View article: 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
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 Open
RLY-2608 biochemical inhibition with liposome substrates
View article: 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 Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia Open
PIK3CA (PI3Kα) is a lipid kinase commonly mutated in cancer, including ∼40% of hormone receptor–positive breast cancer. The most frequently observed mutants occur in the kinase and helical domains. Orthosteric PI3Kα inhibitors suffer from …
View article: Figure S7 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 S7 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 Open
Body weight changes observed in in vivo models upon treatment with RLY-2608
View article: 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 Discovery and Clinical Proof-of-Concept of RLY-2608, a First-in-Class Mutant-Selective Allosteric PI3Kα Inhibitor That Decouples Antitumor Activity from Hyperinsulinemia Open
PIK3CA (PI3Kα) is a lipid kinase commonly mutated in cancer, including ∼40% of hormone receptor–positive breast cancer. The most frequently observed mutants occur in the kinase and helical domains. Orthosteric PI3Kα inhibitors suffer from …
View article: 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 Open
Binding kinetics and potency of [1] towards tailless PI3Kα
View article: 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 Open
Synthesis of mutant-selective allosteric PI3Kα inhibitors
View article: 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 Open
In vitro kinome profile of RLY-2608. RLY-2608 was tested at a concentration of 10 µM by SelectScreen (ThermoFisher Scientific)