Approximately 19% of Europe's population suffers from chronic pain, half of them endure ineffective treatment. Today, most of the research have exacerbated the pathophysiological mechanisms of acute pain, but chronic pain remains to be less studied. A key breakthrough in the chronic pain pathogenicity is the TRPV receptors which are the basis for future development of new classes of analgesics . Study of nociceptive mechanisms. Study of TRPV channel family and its role in receiving, transmitting and modulation of pain. Determination of structure of TRPV channels and activation mechanisms. The role of RTPV in thermoregulation and inflammation. TRPV channels - practical implications of the research. Drugs that act on TRPV channels. The TRPV genes encode transient potential receptor proteins. These channels act as molecular sensors to distinguish pain, temperature, and attenuation. The TRPV1 receptor is the most studied member of the TRPV family. Genetic and pharmacological studies have shown that RTPV1 is an essential component in cellular signaling mechanisms by which the lesion induces thermal hierarchy and hypersensitivity. TRPV channels triggered by physical stimuli, chemicals, toxins, protons, cations, and electricity, are involved in paintful diabetic neuropathy, cancer and inflammation. TRPV agonists (capsaicin, RTX) lead to persistent desensitization, but completely reversible, this demonstrates the therapeutic potential. TRPV antagonists (capsazepine, BCTC) are reported as drugs that reduce the hypersensitivity to neuropathic pain (in preclinical studies). Medicines that target nociceptors have the effect not only for pain relief but also they disrupt the neuroinflammation cycle. Thus, TRPV channels become a new target of pharmacological research, assuming higher efficacy and fewer adverse effects. In present,TRPV agonists (capsaicin, RTX, ALGRX4975 ) and antagonists(capsazepine, BCTC, quinazolinone) are at preclinical animal testing and show effective therapeutic effects.