Innate Pharma has signed a co-development and commercialization agreement with AstraZeneca, along with MedImmune, to accelerate and broaden the development of Innate Pharma's proprietary anti-NKG2A antibody, IPH2201, including in combination with MEDI4736, an anti-PD-L1 immune checkpoint inhibitor developed by MedImmune. Currently in Phase II development, IPH2201 is a potential first-in-class humanized IgG4 antibody.
NKG2A is a checkpoint receptor that inhibits the anti-cancer functions of Natural Killer (NK) and cytotoxic T-cells.
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The financial terms of the signed agreement include cash payments of up to $1.275 billion to Innate Pharma as well as double digit royalties on sales.
The initial payment is $250 million, which includes a consideration for the exclusive global rights to AstraZeneca to co-develop and commercialize IPH2201 in combination with MEDI4736 and access to IPH2201 in monotherapy and other combinations in certain areas.
AstraZeneca will pay to Innate a further $100 million prior to initiation of Phase III development, as well as additional regulatory and sales-related milestones of up to $925 million.
AstraZeneca will book all sales and will pay Innate double-digit royalties on net sales.
The arrangement includes the right for Innate to co-promote in Europe for a 50% profit share in the territory.
The initial development plan includes: Phase II combination clinical trials with MEDI4736 in solid tumors; multiple Phase II trials planned by Innate to study IPH2201 both as monotherapy and in combination with currently approved treatments across a range of cancers; and the development of associated biomarkers.
The combination of IPH2201 with MEDI4736 adds to the broad programme of immuno-oncology combination trials that AstraZeneca and MedImmune have planned and underway.
The studies aim to address multiple immune pathways, harnessing AstraZeneca's own extensive pipeline and working in partnership to explore the significant potential of immunotherapies in transforming the way cancer patients are treated.
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