Oisín Oncology, Inc.
The tumor-suppressor gene p53 is the single most frequently mutated gene in human cancer, being involved in roughly 50% of all invasive tumors and in more than 80% of some of the most difficult-to-treat ones. These mutations are considered “undruggable” because most mutations’ contribution to cancer comes from the absence of a functional protein, with no change in the expression of the gene in most cases, so there is an absence of anything with which a drug might interact.
Oisín’s platform technology uses non-integrating genetic “suicide switches” that overcome this problem by providing the cancer cell with a functional p53 promoter, whose activation by the cancer cell’s primed transcription factors acts as the “on switch” that drives the expression of a cellular apoptotic factor such as caspase 8, eliminating the cancerous cell.
Oisín Biotechnologies SENSolytics
The aging body accumulates senescent cells, which exist in a state of growth arrest and secrete a mixture of inflammatory cytokines, proteinases, growth factors, and other factors that is collectively termed the Senescence-Associated Secretory Phenotype (SASP). Extensive evidence links senescent cells to age- related inflammation, cancer, and other diseases of aging — and conversely, studies show that clearing senescent cells from aging tissues delivers sweeping rejuvenating effects in both otherwise-healthy but aging animals and animal models of age-related disease.
“Senolytic” drugs that destroy senescent cells by inhibiting the cell-survival pathways on which senescent cells differentially rely are now close to reaching the clinic. But these drugs have significant limitations: healthy cells also rely on these same pathways for survival in times of crisis, leading to the risk that senolytic agents will destroy hard-to-replace healthy cells along with the senescent ones when those cells are under stress.
Oisín’s platform technology uses non-integrating genetic “suicide switches” that can be induced and withdrawn from the body entirely at will. In this case, the promoter for p16 (a gene expressed in many senescent cells and not normal ones) acts as the “on switch” that drives the expression of a cellular apoptotic factor, leading to the selective destruction of senescent cells.