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Find Clinical Drug Pipeline Developments & Deals by Ionctura
IOA-289 (cambritaxestat) is a novel, first-in-class inhibitor of autotaxin with a unique binding mode. It is being evaluated for the treatment of pancreatic cancer.
IOA-244 (roginolisib) is a first-in-class small molecule allosteric modulator of PI3Kδ. It is being evaluated for the treatment of metastatic uveal melanoma.
Under the agreement, iOnctura gets exclusive global development rights to IOA-359, a novel oral, small molecule, TGF–β pathway inhibitor that will be evaluated in solid tumors.
The grant will accelerate iOnctura's preclinical investigation of IOA-359, a novel oral, small molecule, TGF–β pathway inhibitor that will be evaluated in solid tumors.
IOA-244 (roginolisib) is a first-in-class, non-ATP-competitive, allosteric modulator of PI3K delta which prevents tumor proliferation and breaks immune tolerance in patients with solid and hematological tumors.
IOA-244 (roginolisib) is a first-in-class, non-ATP-competitive, allosteric modulator of PI3K which prevents tumor proliferation and breaks immune tolerance in patients with solid and hematological tumors.
IOA-244 is a first-in-class semi-allosteric, non-ATP competitive, small molecule PI3Kδ inhibitor which has shown high beneficial tolerability and clinical benefit profile. PI3Kδ over-expression stimulates multiple cancer mechanisms and an oncogenic role in many tumor types.
IOA-289 is the first ATX inhibitor in clinical development for cancer. It is an oral small molecule non-competitive inhibitor with novel binding chemistry and a safe clinical profile. Inhibiting ATX with IOA-289 directly prevents the proliferation of cancer cells.
IOA-289 is an orally dosed small molecule that has been shown preclinically to have a multi-pronged approach to treating cancer, acting directly to prevent proliferation of tumor cells and indirectly to potentiate the actions of the immune system.
IOA-244 is a PI3Kδ specific, orally dosed, small molecule inhibitor that overcomes tumor and stroma induced immune suppression. Its unique chemistry, semi allosteric binding mode and mechanism of action contribute to its unprecedented clinical profile.
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