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Immutep and GlaxoSmithKline Sign Licence Agreement for a Novel Therapeutic Antibody for the Treatment of Autoimmune Diseases
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Immutep and GlaxoSmithKline Sign Licence Agreement for a Novel Therapeutic Antibody for the Treatment of Autoimmune Diseases

Immutep and GlaxoSmithKline Sign Licence Agreement for a Novel Therapeutic Antibody for the Treatment of Autoimmune Diseases
News

Immutep and GlaxoSmithKline Sign Licence Agreement for a Novel Therapeutic Antibody for the Treatment of Autoimmune Diseases

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Immutep S.A. announced today the execution of a licence agreement granting GSK exclusive worldwide rights to ImmuTune(R) 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 disease.
 
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.
 
“We are very pleased to hand over the development of IMP731 to GSK, with its commitment to bringing breakthrough therapies to patients,” said John Hawken, CEO. “For Immutep, the value created through this transaction will enable us to focus our resources on advancing our oncology assets, IMP321 and IMP701. IMP321 is ready for a Phase IIb/III trial in the chemo-immunotherapy of first-line metastatic cancer.”
 
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 (for example production of TNF-a, IL-6, IL-23) 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.
 
Overall, such a targeted therapy, inducing long-term effects with a minimum number of injections is a promising approach in the many autoimmune diseases where self-antigens have activated T-cells, for example, rheumatoid arthritis and multiple sclerosis.

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