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jin-3 is a bioselected oncolytic reovirus mutant derived from the Mammalian Orthoreovirus type 3 Dearing (T3D) strain. It was specifically developed to overcome the requirement for the Junction Adhesion Molecule-A (JAM-A) receptor, which is the primary entry receptor for wild-type reoviruses but is frequently downregulated in advanced or aggressive tumors. By utilizing a JAM-A-independent entry mechanism, jin-3 exhibits expanded tropism, allowing it to infect and replicate in a broader range of cancer cells. The virus functions through direct oncolysis—lytic replication that destroys tumor cells—and by stimulating the host immune system. This stimulation occurs via the induction of immunogenic cell death (ICD), which triggers the expression of interferon-stimulated genes (ISGs) and the release of inflammatory cytokines, potentially converting immunologically "cold" tumors into "hot" tumors. Preclinical studies have demonstrated its efficacy in multiple human prostate cancer models, including castration-resistant prostate cancer (CRPC) and patient-derived xenografts.
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