Cancer growth is driven by a supportive inflammatory tumor micro-environment (“TME”), which provides nutritional and structural support for tumor expansion. The TME is made up of a tightly packed mass of: 1) cancer associated fibroblasts (“CAFs”), 2) tumor-associated macrophages/immune cells (“TAMs”), and 3) cancer itself. The TME’s biophysical properties include regions of varying degrees of hypoxia (low oxygen concentration), acidosis (an excessively acidic condition) and an immunosuppressive milieu.
Current cancer treatment approaches are generally either cytotoxic chemotherapies or focus on targeting one single receptor or one single mutation, which limits their ability to counter an evolvable tumor and its micro-environment
At Immix Biopharma, our SMARxT Tissue-Specific Platform produces Tissue-Specific Therapies (TSTx), which in cancer target all 3 components of the TME simultaneously, severing the critical lifelines between the tumor and its metabolic support using TME Normalization Technology. In inflammation, our Immune Normalization Technology halts the self-sustaining feed-forward loop propagated among 3 key cell-types in inflammatory bowel disease, addressing the root cause of inflammatory pathologies. Our mission is to create an entirely new class Tissue-Specific Therapeutics (TSTx) that personalize treatment to address the complexity of diseases in every patient, starting with oncology & inflammation
Tissue-Specific Therapeutics (TSTx) are a novel class of drugs that treat entire diseased tissues, as exemplified by the tumor micro-environment (TME). TSTx are uniquely capable of addressing the pathologies of complex disease such as cancer and inflammation that are not amenable to traditional one single receptor or one single mutation pharmaceutical development approaches.
Take a deeper dive into TSTx:
TME Normalization Technology. The TME is made up of a tightly packed mass of: 1) cancer associated fibroblasts (“CAFs”), 2) tumor-associated macrophages/immune cells (“TAMs”), and 3) cancer itself. The TME’s biophysical properties include regions of varying degrees of hypoxia, acidosis and an immunosuppressive milieu. As cancer cells outgrow their blood supply, the resulting hypoxia and acidosis shift their metabolism towards glycolysis, lactate and lipids. This, in turn, shapes the responses of proximal fibroblasts and resident immune cells. Fibroblasts begin to secrete lactate that is taken up by nearby cancer cells and consumed as fuel. Lactate in the TME reprograms the macrophages toward the M2 “tolerant” pro-inflammatory phenotype that drives immunosuppression. At the same time, the TME hypoxia produces increased levels of reactive oxygen species that enhance tumorigenicity (tendency to form tumors) and immunosuppressive functions of Treg T-cells, as well as resistance to immune drugs such as PD-1/PD-L1 inhibitors.
Take a deeper dive into TME Normalization Technology:
Immune Normalization Technology. Driving inflammatory bowel pathologies are the interactions between 3 components of the immune synapse: 1) gut-lining enterocytes, 2) gut microbes, and 3) immune cells. Cellular contacts and signaling molecules exchanged between these components activate abnormal inflammatory responses in immune cells driving a self-sustaining feed-forward loop of pathological inflammation in gastrointestinal tissues.
Take a deeper dive into Immune Normalization Technology:
death, not necroptosis
waves of inflammation
sustaining tumor growth
the TME simultaneously
irrespective of the causative
event or genetic predisposition
action has shown promise
in precedent studies