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The main pathogenesis of OA is progressive loss and destruction of articular cartilage, which could eventually lead to joint deformation and immobility 4

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The Benoist 2014 study used the HGF/MET dimerization antagonist Hinge to block Dihexas procognitive activity in scopolamine-impaired rats, with oral Dihexa (2 mg/kg/day) reversing the scopolamine-induced Morris water maze deficit when administered alone but losing effect when co-administered with Hinge [3]

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The molecular mechanisms of HIV-1-related factors in microglial activation and neuroinflammation HIV-1 Tat -mediated microglial activation The persistence of HIV-1 reservoirs in PLWH with virological suppression results in the accumulation of HIV-1 Tat [36]