Creativity and focus power rational design
Our founder, Dr. Michael Curran, is laser focused on cancer. In his early career, he revolutionized the treatment of melanoma by imagining and designing the first FDA-approved immunotherapy combination: CTLA-4 and PD-1 inhibitor, which cured many patients with otherwise terminal disease.
Not willing to stop there, he established the Curran Laboratory in 2012 at MD Anderson Cancer Center with a singular goal: bring the treatment success in immunologically “hot” tumors (eg, melanoma and lung) to immune-resistant “cold” tumors (eg, prostate and colorectal). Numerous resistance mechanisms in these tumor types make this a daunting challenge. And yet, systematically, Dr. Curran has identified key resistance mechanisms and crafted targeted therapeutic interventions.
Dr. Curran has set himself apart by utilizing rational design to overcome key barriers across therapeutic approaches. This focus, this science, this vision form the foundation on which ImmunoGenesis is built.
Learn more about ImmunoGenesisTurn cold tumors hot
Immunosuppressive elements in the tumor microenvironment mean that many tumors evade treatment and are hidden from cancer-destroying immune cells. Tumors are considered “hot” or “cold.” Hot tumors contain many T cells (T-cell inflamed), whereas cold tumors have immunosuppressive elements that exclude T cells. This distinction is crucial because some T cells can recognize and eliminate cancerous cells.
Cold tumors make up the majority of cancers and affect 5 times as many patients as hot tumors. Because cold tumors have unique immunosuppressive characteristics, immunotherapy is only minimally effective in treating these cancers.
At ImmunoGenesis, we aim to turn cold tumors hot to unlock the potential of immunotherapy for more patients.
While traditional approaches and new combination treatments for many cancer types continue to disappoint, ImmunoGenesis is revolutionizing cold tumor treatment. With a deliberate drug development strategy based in cold tumor pathology, we are creating sophisticated therapies that target key mechanisms of immune resistance.
Our team started by targeting the ligands of PD-L1 and PD-L2—rather than the PD-1 receptor—which allowed effector function to be built into the molecule. The goal is to kill the immunosuppressive elements in the tumor microenvironment and facilitate efficacy in cold tumors.
We worked with an innovative antibody design company to create a first-of-its-kind, dual-specific antibody in which both arms bind with clinically relevant affinity to PD-L1 and PD-L2. It took multiple rounds of affinity maturation and more than 3 years to generate an antibody that met our efficacy standards.
Our second clinical program is a hypoxia-reversal agent and primer for enhanced checkpoint inhibition in cold-tumor treatment. Immune T cells typically do not enter hypoxic zones. By reoxygenating the tumor microenvironment, IMGS-101 (evofosfamide) frees T cells to traffic to the tumor and attack cancerous cells.
Dig into our scienceWe are just getting warmed up
The next several years are going to be exciting. We have several programs in the pipeline and a vision for bringing them to life.
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