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d106S-IL12 is a preclinical **replication-defective oncolytic viral therapy** constructed using the herpes simplex virus 1 (HSV-1) d106S vector encoding a single-chain interleukin-12 (IL-12) fusion gene. Designed for **intratumoral delivery**, d106S-IL12 generates a large, localized burst of IL-12 in the tumor microenvironment, resulting in robust secretion of IL-12 and subsequent activation of interferon gamma (IFNγ)-driven anti-tumor immune responses. Preclinical mouse models (notably B16 Nectin1 melanoma) demonstrated d106S-IL12 induces a state of cancer immune equilibrium, wherein tumors neither grow nor regress completely, accompanied by substantial activation of local and systemic immune responses. The single-chain IL-12 format ensures secretion of both subunits (p35 and p40) without competitive antagonism, maximizing immunostimulatory effect. Developer(s) have utilized the system to probe the mechanistic requirements of immune equilibrium—especially the IFNγ axis and adaptive immunity—as well as to investigate the combination of viral vector-based cytokine therapies with standard and experimental cancer immunotherapies[3][5]. There is no evidence of clinical trials in humans; all data are from animal (primarily murine) studies.
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