Immutep and GlaxoSmithKline Sign License Agreement for Imp731
London-based drugmaker GlaxoSmithKline (GSK) and Immutep S.A. (Orsay, France) have signed a license agreement granting GSK exclusive worldwide rights to ImmuTune IMP731 and any other antibodies that deplete LAG-3 positive cells. IMP731 has demonstrated potency at low doses in preclinical models of T-cell mediated inflammation and could represent a new therapeutic approach to the treatment of autoimmune diseases.
London-based drugmaker GlaxoSmithKline (GSK) and Immutep S.A. (Orsay, France) have signed a license agreement granting GSK exclusive worldwide rights to ImmuTune IMP731 and any other antibodies that deplete LAG-3 positive cells. IMP731 has demonstrated potency at low doses in preclinical models of T-cell mediated inflammation and could represent a new therapeutic approach to the treatment of autoimmune diseases.
Under the terms of the agreement, GSK will assume all development responsibility and associated costs for IMP731. Immutep will receive an upfront payment and milestones of up to GBP 64 million (USD 100 million) and is eligible for single-digit, tiered royalties if all objectives are achieved.
IMP731 is a cytotoxic antibody that depletes activated T-cells. Chronically activated T-cells are a major component in many autoimmune diseases. LAG-3 (Lymphocyte Activation Gene-3) is a marker for activated long-lived effector-memory T-cells. Deleting activated pathogenic T-cells rather than simply blocking one of their functions is a new therapeutic approach.
In addition, selective depletion of these pathogenic LAG-3+ T-cells will lead to targeted immunosuppression (i.e., only a subset of activated T-cells will be suppressed, not all T-cells as with corticoids or cyclosporin). This very specific long-lived immunosuppression should lead to higher therapeutic indices compared to classical immunosuppressive agents, with a reduced risk of increased susceptibility to infectious agents, as the pool of resting LAG-3 negative T-cells will be left untouched.
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