Our Science

MorphImmune is founded on the discovery and research of the company’s Scientific Founder, Philip S. Low, PhD, the Presidential Scholar for Drug Discovery and Ralph C. Corley Distinguished Professor of Chemistry at Purdue University. Low, the named inventor of more than 500 patents and patents pending, has created a highly specific targeting technology involving the use of a ligand-linked payload to drug previously undruggable physiological pathways. 

These discoveries have led to the design of targeted drugs to reprogram specific immune cell types (macrophages, T cells, antigen presenting cells, Fc receptor expressing cells, NK cells) for treatment of malignant, CNS, infectious, autoimmune and fibrotic diseases and develop ligand-targeted chemotherapies, radiotherapies, and immunotherapies of cancer.

The human immune system is intimately involved in virtually all diseases, including cancer, microbial infections, fibrotic diseases, diabetes, Crohn’s disease, rheumatoid arthritis, and Alzheimer’s disease. Although modulation of aberrant immune cells has been proposed for remediation of most of these diseases, methods to reprogram malfunctioning immune cells without altering healthy immune cells has been elusive until now. By designing hyper-targeted drugs that home specifically to activated immune cell types, Morphimmune has developed the ability to reprogram malfunctioning macrophages, dendritic cells, NK cells, FcγRIII cells and T cells etc. in pathologic lesions without perturbing their proper functioning counterparts in healthy tissues. This ability to selectively modulate specific immune cell types has proven to be effective in treating models of the above diseases, leading to the development of multiple highly targeted immune-modulating drugs that are currently progressing through the Morphimmune pipeline.

Anti-cancer mechanism of FA-TLR7-1A

Morphimmune develops small molecule targeting ligands for delivering immunomodulating drugs specifically to aberrant immune cells, thereby avoiding the collateral toxicity that occurs when potent modulators of the immune system distribute systemically throughout the body.  For example, in the case of fibrotic diseases, the targeted reprogramming of profibrotic to antifibrotic macrophages specifically halts disease progression without causing detectable systemic toxicity. In a similar manner, selective inhibition of collagen production by myofibroblasts solely in fibrotic tissues suppresses fiber (e.g. collagen) deposition without causing harm to healthy cells.  When applied to cancer, targeted delivery of immune-stimulating drugs to regulatory T cells, myeloid derived suppressor cells or tumor-associated macrophages converts an immunosuppressive tumor microenvironment into a tumoricidal environment, all without altering the biology of properly functioning immune cells. In brief, Morphimmune develops targeted therapeutic agents that selectively morph a disease-promoting immune cell into a disease-suppressing immune cell, thereby remediating aberrant immune cell contributions to such important human pathologies as cancer, rheumatoid arthritis, microbial infections, diabetes, Crohn’s disease, pulmonary fibrosis, multiple sclerosis and Alzheimer’s disease.

Morphimmune has also developed methods to target radiotherapeutic agents specifically to cancer cells and cancer associated fibroblasts (CAFs), thereby concentrating the lethal radioactivity specifically in the solid tumor mass.  Because CAFs may constitute up to 80% of cells in a solid tumor, Morphimmune has developed a targeting ligand for fibroblast activation protein (FAP), a CAF-specific protein, that can bind and internalize FAP-targeted 177Lu radiotherapeutic agents. The consequent concentration of FAP-177Lu in the tumor not only kills the CAFs, but also all cancer cells nearby. Together with several other cancer cell-targeted radiotherapeutic agents, Morphimmune’s FAP-targeted 177Lu radionuclide should enable radiotherapies of most solid tumors.
In summary, Morphimmune has developed methods to target a variety of drugs specifically to diseased cells, thereby avoiding collateral toxicity to healthy cells.  To achieve this specificity, Morphimmune has designed low molecular weight targeting ligands that bind selectively to pathologic cells/aberrant immune cells and has linked these drugs to well-characterized therapeutic or imaging agents.  In the case of cancer, Morphimmune has exploited the up-regulation of fibroblast activation protein (FAP) on cancer-associated fibroblasts to deliver a 177Lu radiotherapeutic agent to the myofibroblasts that constitute a major cell type in almost all solid tumors. Along similar lines, Morphimmune has exploited the expression of folate receptor beta on most tumor-associated macrophages and myeloid-derived suppressor cells to concentrate a folate-TLR7 agonist in these tumor-promoting cells, thereby reprogramming the tumor-supporting cells into tumoricidal cells.   With the development of additional targeting ligands that concentrate attached drugs very selectively into regulatory T cells, profibrotic M2 macrophages, antigen presenting cells, dendritic cells, and natural killer cells, etc., Morphimmune is now well positioned to treat most autoimmune and inflammatory diseases, including pulmonary fibrosis, multiple sclerosis, Crohn’s disease, diabetes, rheumatoid arthritis, Alzheimer’s disease, cirrhosis of the liver, etc.

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