The main insight behind TBT is that not all cortisol is produced by the adrenal glands.  The skin is a giant endocrine gland that has the molecular machinery to produce cortisol, and communicates with the HPA axis to regulate production.

High local cortisol levels degrade a central molecule, gsk3b.  Without enough gsk3b in the cell, another molecule, b-catenin, accumulates in the cell.  Eventually it accumulates in the nucleus.  When it does, the WNT pathway is activated and c-myc, an oncogene, is over produced.  The result is a abnormal differentiation and migration of skin cells, the hallmark of our indications.

Normally, gsk3b plays a pivotal role in degrading

b-catenin, preventing accumulation.

Many things degrade gs3kb, resulting in WNT activation.  High cortisol leads to high levels of glucocorticoid receptor, the main culprit for our indications.

By inhibiting gsk3b phosphorylation, or likewise moving upstream and targeting cortisol, we can reverse this phenotype.  We also have 2 cosmeceutical products in our portfolio targeting deep and superficial wrinkles respectively, with enhanced migration as the underlying mechanism of action.