TNAX101A: Anti-DNAM-1 (CD226) mAb
TNAX101A is a humanized anti-DNAM-1 (CD226) monoclonal antibody (mAb) for the treatment of inflammatory diseases. TNAX101A is a one-of-a-kind “single molecule” anti-inflammatory/fibrotic therapeutic mAb that acts in a pleiotropic, synergistical and rippled way.
It inhibits both innate and adaptive immunity. TNAX101A inactivates effector T cell function, enhances regulatory T cell function, and suppresses a variety of pro-fibrotic/inflammatory cytokines/factors. A surrogate mouse mAb for TNAX101A demonstrates anti-fibrotic/inflammatory effects in various mouse models including an anti-CD40 mAb-induced colitis model, a T-cell transfer colitis model and a bleomycin-induced pulmonary fibrosis model. Unlike existing therapeutics, TNAX101A has a low risk of adverse events especially serious infections because it does not act on healthy tissue or cause excessive immunosuppression. IND-enabling studies are expected to begin soon.
TNAX103A: Anti-CD300A mAb
TNAX103A is a humanized anti-CD300A mAb, which is believed to be an efferocytosis promoter for the treatment of acute ischemic stroke, acute kidney injury, spinal cord injury and acute myocardial infarction.
CD300A expressed on macrophages is a key anti-efferocytic molecule. Dead cells expose phosphatidylserine (PS), which displays “Eat Me” signals, and macrophages induce efferocytosis to clear dead cells. However, PS bound to CD300A expressed on macrophages causes resistance to efferocytosis. TNAX103A normalizes clearance of diseased tissue.
Acute ischemia induces cell death, and dead cells release damage-associated molecular patterns (DAMPs) that produce pro-inflammatory cytokines. Thus, tissue damage is caused by inflammation in acute ischemic dead cells.
When acute ischemic stroke occurs, apoptotic and inflammatory pathways begin over a period of hours to days, leading to neuronal cell death. The penumbra zone, representing the tissue at risk of cell death around the ischemic core, survives for hours to days. The penumbra region may be restored by timely reperfusion and efferocytosis promoters by controlling inflammation induced by cell death. A surrogate mouse mAb for TNAX103A improves neurological scores and histopathological findings in a mouse middle cerebral artery occlusion (MCAO) model.
Furthermore, anti-CD300a mAb improves renal function, damage and fibrosis in mouse ischemia-reperfusion injury model. It ameliorates locomotor ability in mouse spinal cord injury model, too.