Novel AML Therapy


Diffregen is developing a novel immune activating therapeutic to treat Acute Myeloid Leukemia

The Problem

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.


Standard of care chemotherapeutic based treatments are especially hard on the two most afflicted subsets, elderly and young.

FLT-3 and IDH

FLT-3 inhibitors are only applicable to 30% of AML patients, and IDH inhibitors 12%.

Cell Therapy

While adoptive T cell therapies show exiting promise, they are not widely available and not well understood.


  Angiocidin fights AML at its core by halting proliferation of leukemic cells and activating the immune system against cancer.


Angiocidin induces irreversible terminal differentiation in AML cells, reducing the spread of disease and potentiating chemotherapy.

Immune Activation

Angiocidin binds to the DR6 receptor on monocytes, activating them to release immunostimulatory cytokines that activate T-cells.

Anti-tumor activity

In xenograft mouse models, angiocidin works synergistically with chemotherapeutics to increase tumor clearance.


Angiocidin Activation

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.


Myeloid Differentiation

Angiocidin induced terminal differentiation in 4 AML cell lines and 5 primary patient cells in culture. 



Immune Activation

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.


Anti-tumor activity

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.

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