Novel AML Therapy
Diffregen is developing a novel immune activating therapeutic to treat Acute Myeloid Leukemia
The 5 tear survival rate for patients with AML has remained stagnant at 26%. Emerging therapeutics show promise, however these are not available to most patients.
Angiocidin fights AML at its core by halting proliferation of leukemic cells and activating the immune system against cancer.
ANGOCIDIN ACTIVATES THE IMMUNE SYSTEM
Angiocidin binds to the DR6 receptor expressed on immature monocytes, activating the NF-kB pathway and inducing irreversible differentiation into an activated macrophage phenotype.
Activated macrophages release pro-inflammatory cytokines such as IL-2 that activate T-cells and increase their tumor clearing ability.
Proof of Concept
Angiocidin has been shown to induce terminal differentiation in primary patient AML cells and patient derived AML cells lines. In animal models, angiocidin was able to inhibit AML burden by 79% when combined with chemotherapy.
Angiocidin induced terminal differentiation in 4 AML cell lines and 5 primary patient cells in culture.
Angiocidin was shown to induce macrophages to release of a host of pro-inflammatory cytokines in monocytes, and is able to activate t-cell in co-culture.
In AML xenograft mouse studies, angiocidin was able to reduce AML in the bone marrow by 63% (more than chemotherapy alone), and 79% in combination with chemotherapy.