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Research demonstrates that TB-500 forms functional complexes with PINCH-1 and integrin-linked kinase (ILK) that can inhibit TNF--induced NF-B activation through blocking RelA/p65 translocation, providing rapid suppression of inflammatory transcriptional programs

Patients with HT who received replacement with levothyroxine (L-T4) did not always achieve clinically significant results, which requires additional therapeutic agents ( The significant prevalence of AITD, a long latent period and the involvement of autoimmune processes in their occurrence, development of concomitant diseases, insufficient effectiveness of the main pharmacotherapy, and a decrease in the quality of life of patients require the development of adequate approaches for the correction of immune processes in order to prevent and treat diseases