TRPV3 is a temperature-sensitive transient receptor potential (TRP) ion channel which functions as a Ca⁺⁺ cation channel.

TRPV3 is a master regulator of skin homeostasis genetically validated in humans.

TRPV3 gain-of-function mutations lead to a severe dermatology conditions such as Keratoderma and Ichthyosis, characterized by skin dysregulation, itch and pain.

TRPV3 is highly expressed and over – active in various lesioned hyperkeratotic conditions.

TRPV3 knockout animals exhibit a markedly suppressed itch-associated behavior (Yoshioka et al 2012).

Activation of PAR2 triggers itch through intracellular PLC- Ca+2 signaling which is suppressed by TRPV3 inhibition Jiahui Zhao 2020.

Excessive activation of TRPV3 in keratinocytes lead to the release pruritogenic substances.

Warmth-evoked itch in keratinocytes through TRPV3 can be reduced by TRPV3 antagonists.

Skin barrier deconstruction is seen in LSC, TRPV3 inhibition has the potential to restore skin barrier.

Normalize skin differentiation and reduce hyperkeratosis and itch.


Kamari’s proprietary molecule, KM-001 is a TRPV3 inhibitor that addresses both the molecular and local damage to the skin by regulating Ca⁺⁺ influx into the cell.

Molecular Damage
In animal models, KM-001 normalized Ca⁺⁺ influx and positively impacted the structure of the skin; normalizing keratinocytes, reducing inflammation and restoring the sensation of itch to it’s normal protective status.

Local Damage
In preclinical studies, the use of KM-001 led to a reduction in scratching, decrease in local harm to tissue, and breaking the cycle of chronic debilitating itch.