TTX 334e Endometriosis

What if an antigen were expressed in both malignant (ovarian) and benign (endometriosis and fibrotic) tissues yet on the cell surface of normal cells it is absent?

What if this antigen was a key mechanistic player for cell survival?

What would it mean if the therapeutics candidate TTX334e could reduce endometriosis tissue, reduce pain, and minimize need for laparoscopic surgeries while leaving healthy tissue unharmed?  

Oxidative stress and inflammation are linked to the pathogenesis of endometriosis. Myeloperoxidase (MPO) is a proinflammatory enzyme and a marker for neutrophil activation and oxidative stress. Temple has identified the target responsible for cell proliferation and inhibiting apoptosis. It is a novel target which appears to have not been drugged before. The target is on the ER alpha pathway. Endometriosis is an estrogen-dependent disease. The biologically active estrogen, estradiol, aggravates the pathological processes (e.g., inflammation and growth) and the symptoms (e.g. pain) associated with endometriosis.

Endometriosis cell killing or apoptosis was induced when MPO was inhibited through this novel target, supporting novel mechanism and increasing the possibility of the FIRST NON-HORMONAL therapy for millions of women.  

Preclinical Results TTX 334e Endometriosis

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