Our new 3D animation explains in quite a detail the mechanism of action of a novel (second-generation) TNF inhibitor – INB03, also known as XPro1595.
Tumor Necrosis Factor is an APEX driver of both the “good” and “bad” aspects of immune function.
The “good” TNF is membrane-bound and provides various levels of support, many critical, to cells throughout the body. The “bad” TNF, or soluble TNF, is generated when membrane-bound TNF is enzymatically cleaved. It is this soluble form of TNF that causes chronic inflammation and disease.
INB03 is a novel TNF blocker that only targets the “bad” TNF. The effects of “bad” TNF occur only when three identical soluble TNF proteins come together as a trimer and bind TNF receptors. INB03 mimics these TNF proteins. As a result, INB03 can freely exchange and form trimers with native TNF proteins. However, INB03 has a mutation in the receptor-binding domain, which prevents trimers containing INB03 and native soluble TNF from binding to TNF receptors. This stops chronic inflammation. Because INB03 uses a novel dominant-negative technology, only one INB03 molecule is required in a trimer to neutralize native soluble TNF. The “good” TNF is bound to the membrane, making it impossible for INB03 to exchange.
Due to this selectivity, INB03 stops chronic inflammation and polarizes TNF activity toward its supportive functions, which has implications in oncology and neurodegenerative diseases such as Alzheimer’s disease.
Learn more at inmunebio.com