TY - JOUR
T1 - A phase I/IB trial of the vegfr-sparing multikinase ret inhibitor RXDX-105
AU - Drilon, Alexander
AU - Fu, Siqing
AU - Patel, Manish R.
AU - Fakih, Marwan
AU - Wang, Ding
AU - Olszanski, Anthony J.
AU - Morgensztern, Daniel
AU - Liu, Stephen V.
AU - Cho, Byoung Chul
AU - Bazhenova, Lyudmila
AU - Rodriguez, Cristina P.
AU - Doebele, Robert C.
AU - Wozniak, Antoinette
AU - Reckamp, Karen L.
AU - Seery, Tara
AU - Nikolinakos, Petros
AU - Hu, Zheyi
AU - Oliver, Jennifer W.
AU - Trone, Denise
AU - McArthur, Katherine
AU - Patel, Rupal
AU - Multani, Pratik S.
AU - Ahn, Myung Ju
N1 - Funding Information:
A. Drilon is a consultant/advisory board member for Ignyta, Genentech, BeiGene, Hengrui Therapeutics, Exelixis, Bayer, Roche, Loxo Oncology, TP Therapeutics, AstraZeneca, Pfizer, Blueprint, Takeda/Ariad, and Helsinn Therapeutics and has received Pocket Oncology royalties from Wolters Kluwer. M. Fakih reports receiving commercial research grants from AstraZeneca, Novartis, and Amgen, has received honoraria from the speakers bureaus of Amgen, Taiho,
Funding Information:
A. Drilon is supported by the NIH award P30 CA008748. This study was sponsored by Ignyta.
Publisher Copyright:
© 2018 American Association for Cancer Research.
PY - 2019/3/1
Y1 - 2019/3/1
N2 - RET fusions are oncogenic drivers of various tumors, including non–small cell lung cancers (NSCLC). The safety and antitumor activity of the multikinase RET inhibitor RXDX-105 were explored in a phase I/Ib trial. A recommended phase II dose of 275 mg fed daily was identified. The most common treatment-related adverse events were fatigue (25%), diarrhea (24%), hypophosphatemia (18%), maculopapular rash (18%), and nonmaculopapular rash (17%). In the phase Ib cohort of RET inhibitor–naïve patients with RET fusion–positive NSCLCs, the objective response rate (ORR) was 19% (95% CI, 8%–38%, n = 6/31). Interestingly, the ORR varied significantly by the gene fusion partner (P < 0.001, Fisher exact test): 0% (95% CI, 0%–17%, n = 0/20) with KIF5B (the most common upstream partner for RET fusion–positive NSCLC), and 67% (95% CI, 30%–93%, n = 6/9) with non-KIF5B partners. The median duration of response in all RET fusion–positive NSCLCs was not reached (range, 5 to 18+ months). SIGNIFICANCE: Although KIF5B-RET is the most common RET fusion in NSCLCs, RET inhibition with RXDX-105 resulted in responses only in non– KIF5B–RET- containing cancers. Novel approaches to targeting KIF5B-RET- containing tumors are needed, along with a deeper understanding of the biology that underlies the differential responses observed.
AB - RET fusions are oncogenic drivers of various tumors, including non–small cell lung cancers (NSCLC). The safety and antitumor activity of the multikinase RET inhibitor RXDX-105 were explored in a phase I/Ib trial. A recommended phase II dose of 275 mg fed daily was identified. The most common treatment-related adverse events were fatigue (25%), diarrhea (24%), hypophosphatemia (18%), maculopapular rash (18%), and nonmaculopapular rash (17%). In the phase Ib cohort of RET inhibitor–naïve patients with RET fusion–positive NSCLCs, the objective response rate (ORR) was 19% (95% CI, 8%–38%, n = 6/31). Interestingly, the ORR varied significantly by the gene fusion partner (P < 0.001, Fisher exact test): 0% (95% CI, 0%–17%, n = 0/20) with KIF5B (the most common upstream partner for RET fusion–positive NSCLC), and 67% (95% CI, 30%–93%, n = 6/9) with non-KIF5B partners. The median duration of response in all RET fusion–positive NSCLCs was not reached (range, 5 to 18+ months). SIGNIFICANCE: Although KIF5B-RET is the most common RET fusion in NSCLCs, RET inhibition with RXDX-105 resulted in responses only in non– KIF5B–RET- containing cancers. Novel approaches to targeting KIF5B-RET- containing tumors are needed, along with a deeper understanding of the biology that underlies the differential responses observed.
UR - http://www.scopus.com/inward/record.url?scp=85063573548&partnerID=8YFLogxK
U2 - 10.1158/2159-8290.CD-18-0839
DO - 10.1158/2159-8290.CD-18-0839
M3 - Article
C2 - 30487236
AN - SCOPUS:85063573548
SN - 2159-8274
VL - 9
SP - 384
EP - 395
JO - Cancer Discovery
JF - Cancer Discovery
IS - 3
ER -