CatalYm to Present Data on Targeting Novel Checkpoint GDF-15 for Immunotherapy of Cancer at the AACR Annual Meeting 2020


MUNICH, Germany, June 18, 2020 (GLOBE NEWSWIRE) -- CatalYm GmbH, a biopharmaceutical company developing novel cancer immunotherapies, today announced that two abstracts identifying a novel immunoregulatory role for Growth-and-Differentiation Factor 15 (GDF-15) and its effective neutralization by CatalYm’s CTL-002 antibody in cancer have been selected for presentation during the American Association for Cancer Research (AACR) Virtual Annual Meeting II on June 22 – 24, 2020.

Tumor-derived GDF-15 suppresses T-lymphocyte recruitment to the tumor microenvironment” [Abstract #5597, Poster #8]
Session: Inflammation, Immunity, and Cancer / Modifiers of the Tumor Microenvironment 2 [PO.IM02.21]
Date and Time: Monday June 22, 2020 9:00 AM to 6:00 PM
Location: Virtual Meeting II: E-Posters [aacr.org]

The abstract describes in vitro and in vivo data, which demonstrate that tumor cells secrete GDF-15 to block T-cell entry into tumor tissue. Neutralizing GDF-15 with CatalYm‘s proprietary antibody (CTL-002) restored the ability of CD8+ T-cells to enter the tumor microenvironment and restored anti-PD1 activity in an anti-PD1 refractory setting.

“Identifying GDF-15 as potential novel immunotherapeutic target linked to immune cell exclusion in tumors and resistance to anti-PD-1 treatment [Abstract #2161, Poster #22]
Session: Adaptive Immunity to Tumors [PO.IM01.01]
Date and Time: Monday June 22, 2020; 9:00 AM – 6:00 PM
Location: Virtual Meeting II: E-Posters [aacr.org]

The abstract reveals that melanoma patients with high GDF-15 levels have significantly shorter survival and are less likely to respond to anti-PD1 therapy. In addition, intratumoral GDF-15 levels in human melanoma correlated inversely with CD3+ and CD8+ T cell infiltration. Consequently, GDF-15 may serve as a predictive biomarker for anti-PD1 response and potentially represents a novel target in the immunotherapy of cancer to improve tumor immune cell infiltration and response to cancer immunotherapy.

Dr. Manfred Rüdiger, CEO of CatalYm, states: “Our data show that GDF-15 is a novel checkpoint factor secreted by tumors. GDF-15 serves as T cell repellent and may cause low or no response to modern immunotherapies. Neutralizing GDF-15 with our CTL-002 antibody is a novel promising approach to increase response rates of cancer immunotherapies and overall survival of cancer patients.”

CTL-002 is set to enter clinical development during 2020.

About CatalYm

CatalYm is a biopharmaceutical company developing novel cancer immunotherapies targeting Growth-and-Differentiation Factor 15 (GDF-15). Apart from its established role in cachexia, GDF-15 has been associated with immunosuppression in tissues and tumorsi and a rapidly growing body of literature supports the concept that GDF-15 is a major T cell repellent. CatalYm aims to neutralize GDF-15 to turn “cold” tumors “hot” and thereby substantially improving the efficacy of established immunotherapy such as anti-PD1/-PD-L1 checkpoint inhibitors. The company’s lead product candidate CTL-002, a neutralizing GDF-15 antibody, is set to enter clinical development in H2 2020.

The Company was founded in 2016 as a spin-off from Wuerzburg University. CatalYm is led by a seasoned senior executive team with substantial I/O drug development as well as deal making experience and backed by international venture capital investors.

About CTL-002

CTL-002 is a humanized, hinge-stabilized IgG4 monoclonal antibody targeting Growth Differentiation Factor-15 (GDF-15), a remote member of the transforming growth factor β superfamily of cytokines, that is associated with poor outcome and reduced overall survival in a multitude of cancer types and has been linked to immunosuppression in the tumor microenvironment.

Contact
CatalYm GmbH
Dr. Manfred Rüdiger, CEO
Am Klopferspitz 19
82152 Martinsried, Planegg
Germany
info@catalym.com
Media Inquiries
MC Services AG
Katja Arnold, Julia von Hummel, Shaun Brown
T: +49(0)89 21022880
catalym@mc-services.eu

                                                          

i Front. Immunol. 11:951. doi: 10.3389/fimmu.2020.00951