Reshaping the future for patients with non-immunogenic tumors
By pioneering targeted immune stimulation, our unique mode of action, we develop a groundbreaking class of cancer therapies that will form the future treatment paradigm for non-immunogenic tumors.
Science
IFNy is a potent driver of immune infiltration in cold tumors
Cold tumors need new therapies
Immunotherapies such as checkpoint inhibitors are highly efficient in many solid tumor types. However, immune cells need to be present in the tumor micro-environment (TME) for these immunotherapies to work. Cold tumors, or non-immunogenic tumors, secrete suppressive molecules and mutate their cellular markers which prevents immune cells from entering the TME, rendering immunotherapies ineffective.
IFNγ injections are potent but dangerous
Interferon gamma (IFNγ) is a powerful anti-tumor cytokine that has been linked in the clinic to induce immune cell infiltration and activation in the TME. However, previous attempts to use recombinant IFNγ therapeutically have resulted in side-effects due to rapid spikes in systemic cytokine levels and limited efficacy due to low accumulation in the TME.
TIMS enables IFNγ potency in a safe way
Cymab’s novel Targeted Immune Stimulation (TIMS) technology solves this by binding free, endogenous IFNγ with our novel antibody which prolongs IFNγ half-life and hence its exposure to the tumor. IFNγ levels in the tumor are thereby increased without side-effects associated with rapid raising of systemic IFNγ concentrations. Tumor accumulation can be further increased via addition of a tumor associated antigen-targeting domain to our antibody, when needed. TIMS transforms cold tumors into immune-active sites, enabling tumor cell killing as a monotherapy and significantly enhancing checkpoint inhibitor efficacy in combination therapy.
Technology
Our Targeted Immune Stimulation (TIMS) technology accumulates endogenous IFNγ in a novel way
1.
Binding the body’s own IFNγ
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When injected into the blood stream, our TIMS antibody binds to circulating IFNγ with one of its binder arms. Binding to IFNγ is optimised to promote IFNγ’s anti-cancer activity at the tumor site.
2.
IFNγ delivery to tumor cells
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Bound IFNγ accumulates at the tumor site due to inherent accumulation patterns of antibodies in tumor tissues. Addition of a second tumor associated antigen (TAA) binder arm has the potential to further increase tumor accumulation when needed.
3.
Tumor immune cell infiltration
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The bound IFNγ engages with its receptor on tumor cells to initiate chemokine (CXCL9-10) secretion and MHC-I expression which attracts immune cells to the tumor, facilitating tumor killing. The bound IFNγ also engages with infiltrating immune cells which alters the tumor microenvironment and further stimulates the anti-tumor response. Once the immune response is initiated our TIMS antibodies moreover capture locally released IFNγ which potentiates the anti-tumor response. In addition to the anti-tumor effect, immune cell infiltration also enables previously ineffective immunotherapies to work again.
Pipeline
A novel IFNγ binder with targeting versatility
In a mono-specific format, endogenous IFNγ is bound which prolongs its half-life and hence exposure to the tumor. In this format, our antibody enables tumor agnostic therapy for tumors lacking defined TAAs or with inherent antibody accumulating structures (e.g. liver tumors).
In a bi-specific format, IFNγ levels in the tumor are further increased and tumor exposure to IFNγ sustained via antibody binding to a tumor associated antigen (TAA). In this format, our antibody enables tumor specific therapy for tumors with well-defined and abundant TAA expression that might require higher therapeutic IFNγ levels. Due to the modular format, different TAAs can be chosen to target a wide range of cold tumor types.
INDICATION
Cold tumor
agnostic
TARGET
IFNγ
FORMAT
Mono
PHASE
CYM-monoAb
Un-targeted mono-specific antibody format that binds and delivers IFNγ to cold tumors in an indication agnostic manner.
INDICATION
Prostate
tumors
TARGET
IFNγ + PSMA
FORMAT
Bi
PHASE
CYM-biAb (PSMA)
Targeted bi-specific antibody format that binds and delivers IFNγ to cold prostate tumors via PSMA targeting. PSMA is an antigen overexpressed on prostate tumor cells compared to healthy tissue.
Team
Experienced Leadership Team, Leading Advisors
Core team
Board of directors
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