Immunotherapy in oncology is becoming a clinical reality and raises hope for patients by mobilizing their own immune defense to fight against cancer.   MENK (small peptides triggering immune response) are optimized. They have been selected and modified for a stronger binding with immune response receptors causing an increase in circulating cytotoxic T cells (CD8+/TH1) and natural killer cells (“NK cells”) MENK triggers a stronger immune response and target tumor growth associated antigens expressed in several cancers.

The role of opioid peptides in cancer cell growth has been examined in both tissue culture models and in vivo studies. These studies have revealed that the pentapeptide MENK, or IRT-101, is the most potent opioid peptide that influences DNA synthesis and cell growth. Because of MENK’s ability to have a direct impact on the growth factor action, MENK has also been termed Opioid Growth Factor (“OGF”). MENK or OGF is an endogenous opioid peptide that interacts with the OGFr, which delays the cell cycle by modulating cyclin-dependent inhibitory kinase pathways. The OGF-OGFr axis is an inhibitory pathway that plays a role in the onset and progression of autoimmune diseases and cancer.

The OGF-OGFr peptide and receptor have been detected in a wide variety of cancers, including thyroid cancer (e.g. follicular-derived thyroid cancers), ovarian cancer, triple negative breast cancer, hepatocellular carcinoma, squamous cell carcinoma of the head and neck, pancreatic cancer, renal cancer, neuroblastoma, and colon cancer.

It has been shown in a number of research studies that the OGF-OGFr axis can be directly targeted by the administration of exogenous MENK. MENK, at suitable doses, can inhibit cancerous cell growth by MENK’s direct interaction with OGFr creating a competitive inhibition profile and subcellular location that is different from other well-known opioid receptors [mu (µ), delta (δ) and kappa (κ)]. The other “classic” opioid receptors [mu (µ), delta (δ) and kappa (κ)] have not been found to have any impact on cell growth; thus there is specificity in the MENK-OGFr interaction, which regulates cell proliferation. MENK has been shown to act directly on cells to inhibit proliferation as documented by tissue culture models that lack feedback loops or whole animal autocrine systems. Studies in vitro have shown that MENK has no effects on the apoptosis pathways or cell differentiation. The chemokine system is more likely a more recent evolutionary branch of other chemo-attractant systems in the body such as the complement system.

Research results to date indicate that MENK, at suitable doses, in addition to inhibiting cancerous cell growth, can also boost the immune system through the following possible mechanisms:

  • increasing proliferation and functional activities of CD4+T-cells and CD8+T-cells which will play a role in anti-virus and anti-tumor activities;
  • increasing maturation of dendritic cells which will initiate and intensify T-cell responses;
  • increasing secretion of cytokines such as IL-2, TNF, IL-12 and IFN-g which will amplify the T-cell response and mediate interaction among immune cells, forming a modulated and balanced immunity;
  • increasing functions of macrophages, resulting in enhanced cellular immunity through secreting a set of cytokines; and
  • increasing activity of NK cells which have the ability to kill cancer cells and virus-infected cells.