Our lead RAF program, KIN 2787 is a small molecule kinase inhibitor targeting specific classes of BRAF kinase alterations (Class II and Class III) that characterize subsets of melanoma, lung cancer, and other solid tumors. As a pan-RAF kinase inhibitor, KIN-2787 inhibits CRAF, a critical effector of oncogenic signaling in NRAS-mutant melanoma. While three BRAF targeted kinase inhibitor drugs targeting the Class I BRAF alterations have been approved by the FDA, no targeted therapies have been approved for Class II or Class III BRAF alteration-driven cancers or NRAS-mutant driven melanoma
Patients with Class II or Class III BRAF alterations and NRAS-mutant melanoma do not respond to existing approved targeted therapies, have few treatment options available to them, and consequently have a poor prognosis. Initially, we plan to develop KIN-2787 for the treatment of patients with melanoma and non-small cell lung cancer (NSCLC) subpopulations with Class II or Class III BRAF alterations that include specific BRAF point mutations (other than BRAF V600E), BRAF insertions/deletions (indels) and BRAF gene fusion events as well as for the treatment of patients with NRAS-mutant melanoma. We expect that KIN-2787 may provide substantial clinical benefit to these cancer patients who are inadequately served by current therapies. We are currently evaluating the safety and tolerability of KIN-2787 in a first-in-human dose-escalation study in adults with BRAF-mutated advanced or metastatic solid tumors and NRAS-mutated advanced or metastatic melanoma both as a monotherapy and in combination with binimetinib for NRAS-mutant melanoma (KN-8701).
More information can be found on ClinicalTrials.gov at: https://www.clinicaltrials.gov/ct2/show/NCT04913285
69
Our lead RAF program, KIN 2787 is a small molecule kinase inhibitor targeting specific classes of BRAF kinase alterations (Class II and Class III) that characterize subsets of melanoma, lung cancer, and other solid tumors. As a pan-RAF kinase inhibitor, KIN-2787 inhibits CRAF, a critical effector of oncogenic signaling in NRAS-mutant melanoma. While three BRAF targeted kinase inhibitor drugs targeting the Class I BRAF alterations have been approved by the FDA, no targeted therapies have been approved for Class II or Class III BRAF alteration-driven cancers or NRAS-mutant driven melanoma
Patients with Class II or Class III BRAF alterations and NRAS-mutant melanoma do not respond to existing approved targeted therapies, have few treatment options available to them, and consequently have a poor prognosis. Initially, we plan to develop KIN-2787 for the treatment of patients with melanoma and non-small cell lung cancer (NSCLC) subpopulations with Class II or Class III BRAF alterations that include specific BRAF point mutations (other than BRAF V600E), BRAF insertions/deletions (indels) and BRAF gene fusion events as well as for the treatment of patients with NRAS-mutant melanoma. We expect that KIN-2787 may provide substantial clinical benefit to these cancer patients who are inadequately served by current therapies. We are currently evaluating the safety and tolerability of KIN-2787 in a first-in-human dose-escalation study in adults with BRAF-mutated advanced or metastatic solid tumors and NRAS-mutated advanced or metastatic melanoma both as a monotherapy and in combination with binimetinib for NRAS-mutant melanoma (KN-8701).
More information can be found on ClinicalTrials.gov at: https://www.clinicaltrials.gov/ct2/show/NCT04913285
62
Our FGFR program, KIN-3248 is a small-molecule kinase inhibitor that target cancer-associated alterations in FGFR2 and FGFR3 genes, which are among the most commonly identified oncogenic drivers detected in solid tumor cancers. KIN-3248 aims to address the primary driver-alteration and clinically observed and predicted FGFR 2/3 mutations that drive resistance to current FGFR2- and FGFR3-targeted therapies in intrahepatic cholangiocarcinoma (ICC) and urothelial carcinoma (UC). In preclinical studies, we have observed inhibitory activity across a broad range of clinically relevant mutations that drive acquired resistance. We believe that by addressing these mutations and broadly covering FGFR isoforms, we may be able to meaningfully increase the duration of response (DoR).
We are currently evaluating the safety and tolerability of KIN-3248 in a first-in-human dose-escalation study in adults with advanced tumors harboring FGFR2 and/or FGFR3 gene alterations.
More information can be found at ClinicalTrials.gov at: https://clinicaltrials.gov/ct2/show/NCT05242822.
62
We are also advancing a number of other small molecule development programs, including a CDK12 inhibitor. CDK12 is an essential regulator of DNA damage response genes against which no targeted therapies are currently approved or, to our knowledge, in clinical development. We expect to develop a CDK12 candidate to target the treatment of ovarian carcinoma (OC), triple-negative breast cancer (TNBC), and metastatic castration-resistant prostate cancer (mCRPC). CDK12 along with our other small molecule development programs expand our penetration into cancer types not covered by existing targeted therapies.
35
We are actively engaged in discovery-stage programs investigating multiple undisclosed programs targeting key molecular drivers in cancer.
17
This is a placeholder. It's hidden from the grid/chart , but necessary to display the filter option until real projects have this category. Keep the category "Hidden" enabled.
This is a placeholder. It's hidden from the grid/chart , but necessary to display the filter option until real projects have this category. Keep the category "Hidden" enabled.
This is a placeholder. It's hidden from the grid/chart , but necessary to display the filter option until real projects have this category. Keep the category "Hidden" enabled.
