SOURCE: Kadmon Corporation

Kadmon Corporation

November 03, 2015 08:30 ET

Kadmon Corporation Presents Preclinical Data on Immuno-Oncology Anti-PD-L1/IL-15 Fusion Protein at AACR-NCI-EORTC Symposium

Novel Immuno-Oncology Agent Stimulates Immune Response in Local Microenvironment for Enhanced Anti-Tumor Effect

NEW YORK, NY--(Marketwired - Nov 3, 2015) - Kadmon Corporation, LLC today announced preclinical data demonstrating the potential of a novel anti-PD-L1/IL-15 fusion protein, KD033, for the treatment of cancer. The data demonstrate that treatment with KD033 activates a potent immune response in the tumor microenvironment, effectively controlling tumor progression with minimized potential adverse effects. The data will be presented in a poster session at the 2015 AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics Conference, taking place November 5-9, 2015, in Boston, MA. 

Cancer immunotherapy aims to harness the body's immune system to attack tumor cells. Anti-PD-L1 antibodies, which appear to restore the immune system's ability to fight tumor cells, have shown remarkable efficacy but have limited clinical utility in certain patients. Immunostimulatory cytokines such as IL-15 lack proper targeting potential and invoke systemic toxicities. KD033 overcomes these hurdles by simultaneously inhibiting the PD-L1 pathway to reduce immune checkpoint blockade and directing an IL-15-stimulated immune response into the tumor microenvironment.

The data demonstrate that KD033 treatment suppressed tumor growth in aggressive tumor models and prolonged the survival of tumor-bearing mice, with significantly less cytokine-related toxicity compared to non-targeted IL-15 cytokine therapy in vivo. KD033 has favorable thermal stability and can be efficiently expressed in mammalian cells, with high affinity to PD-L1 and the ability to stimulate T-cell and NK (natural killer) cell activity through the IL-15 pathway. These results indicate that KD033 is capable of targeting IL-15-stimulated innate and adaptive immunity into local tumor sites and may have greater efficacy than single-agent PD-L1 inhibitors. 

"KD033 combines the effects of two complementary immuno-oncology approaches to restore innate immunity while stimulating an adaptive anti-tumor response, achieving greater efficacy than single-agent therapy," said Yan Wu, Ph.D., Senior Director, Antibody Research at Kadmon. "These results support our plans to research KD033 in humans, particularly in patients not responding to anti-PD-1/PD-L1 antibodies." 

"At Kadmon, we are developing a portfolio of bi-functional and fusion protein immuno-oncology agents that we believe represent the next generation of cancer therapy," said Larry Witte, Ph.D., Executive Vice President, Research and Development at Kadmon. "Our most advanced candidate from this program, KD033, has shown promising results and we look forward to advancing this innovative therapeutic candidate into the clinic."

About Kadmon Corporation
Kadmon Corporation, LLC is a fully integrated biopharmaceutical company focused on developing innovative products for significant unmet medical needs. We have a diversified product pipeline in oncology, autoimmune and fibrotic diseases, metabolic disease and certain monogenic diseases. For more information, visit www.kadmon.com.

This press release contains forward-looking statements. These forward-looking statements are based on management's expectations and are subject to certain factors, risks and uncertainties that may cause actual results, outcome of events, timing and performance to differ materially from those expressed or implied by such statements. The information contained in this press release is believed to be current as of the date of original issue. Kadmon expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in our expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.

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    Ellen Tremaine
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