Deep Expertise in Chemistry and Structure-based Drug Design Drives Pipeline of Highly Selective Compounds

At Kinnate, we specialize in developing innovative cancer treatments by targeting specific proteins called kinases. Kinase inhibition has been proven effective in fighting cancer for nearly 20 years, and we have a skilled team dedicated to discovering new drugs and advancing them to clinical trials.

Our approach focuses on creating unique programs that specifically target validated drivers of cancer. When designing our molecules, we prioritize four key factors: high selectivity (to minimize off target activity), optimized pharmaceutical properties (ensuring the drug works well in the body), broad coverage of genetic alterations (addressing different genetic changes in cancer cells), and the ability to overcome resistance or penetrate the brain.

Our goal is to develop drug candidates that have a therapeutic window, meaning they provide lasting and meaningful clinical responses to help patients. We focus on three specific patient populations:

Patients with cancers that have known genetic drivers but currently lack targeted therapies.
Patients with tumors that are well-characterized genetically and have intrinsic resistance to existing treatments.
Patients whose tumors develop resistance to current therapies over time.

By focusing on these well-defined patient populations, we believe we can streamline the development process and increase our chances of success. We have built strong relationships with precision medicine cancer centers and research institutions, allowing us to leverage advancements in genomic profiling and deepen our understanding of specific cancer drivers.

Everyone at Kinnate is deeply committed to making a difference in the lives of patients with cancer by developing effective and targeted treatments based on cutting-edge research and collaboration with leading experts in the field.

A Focused Pipeline

We have developed a proprietary portfolio of small molecule candidates targeting validated drivers of cancer.

RAF / exarafenib Monotherapy

Phase 1b

Kinnate is exploring strategic alternatives for is exarafenib (KIN 2787) as a monotherapy agent.

BRAF-Driven Advanced Adult Solid Tumors

Exarafenib Monotherapy
Pan-RAF

RAF / exarafenib Combination

Phase 1a

Exarafenib (KIN-2787) is an orally administered, potent and selective investigational small molecule pan-RAF inhibitor. KN-8701 is an ongoing, global Phase 1 clinical trial (NCT04913285) evaluating exarafenib in patients with advanced solid tumors harboring BRAF-altered and/or who have NRAS mutant melanoma. KN-8701 contains a two-part dose escalation: Part A1 evaluated exarafenib as a monotherapy across BRAF alterations and tumor types, and Part A2 is evaluating exarafenib in combination with binimetinib, a MEK inhibitor. Part B, dose expansion, is evaluating exarafenib monotherapy at 300 mg bid in patients with BRAF-altered cancers including lung cancer, melanoma and other solid tumors. Watch: Exarafenib Mechanism of Action As of September 18, 2023, exarafenib plus binimetinib was generally well-tolerated in two dose cohorts and cleared by a dose review committee. In the fourth quarter of 2023, the Company intends to select two doses for further development.

Advanced NRAS Mutant Melanoma

Exarafenib Combination
Pan-RAF

Exarafenib (KIN-2787) is an orally administered, potent and selective investigational small molecule pan-RAF inhibitor. Unlike currently available treatments that target only Class I BRAF kinase mutations, exarafenib is designed to target BRAF Class II and Class III alterations, where it has the potential to be a first-line targeted therapy, in addition to covering BRAF Class I alterations, and as a potential treatment for NRAS mutation-positive melanoma. KN-8701 is an ongoing, global Phase 1 clinical trial (NCT04913285) evaluating exarafenib in patients with advanced solid tumors harboring BRAF Class I, II and III alterations, and/or who have NRAS mutant melanoma. KN-8701 contains a two-part dose escalation: Part A1 is evaluating exarafenib as a monotherapy across BRAF alterations and tumor types, and Part A2 is evaluating exarafenib in combination with binimetinib, a MEK inhibitor. Part B, dose expansion, is evaluating exarafenib at the recommended dose and schedule in patients with BRAF-altered cancers including lung cancer, melanoma and other solid tumors1.

FGFR2/3 / KIN-3248

Phase 1a

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). Kinnate is currently exploring strategic alternatives for its KIN-3248 program.

Naïve + Pre-treated FGFR2/3 Driven Advanced Adult Solid Tumors

KIN-3248
FGFR2/3- Driven

KIN-8741

IND-Enabling

KIN-8741 is designed to be a highly selective c-MET inhibitor with broad mutational coverage, including acquired resistance mutations, in solid tumors driven by exon 14-altered and/or amplified c-MET. A primary focus for KIN-8741 is on non-small cell lung cancer, where the c-MET exon 14 alteration serves as the primary driver alteration. Kinnate expects to file an IND application for KIN-8741 with the U.S. Food and Drug Administration (FDA) in the fourth quarter of 2023.

c-Met-Driven Advanced Adult Solid Tumors

KIN-8741
c-MET, Covers Acquired Resistance

CDK4

Discovery

Kinnate is exploring drug candidates (DC) for a potentially brain-penetrant, selective CDK4 inhibitor and expects to nominate a DC in the fourth quarter of 2023.

Adult Solid Tumors

CDK4