Abstract: A small molecule TNF-? inhibitor is disclosed. The compound has an activity of inhibiting the formation of a TNF-? homotrimer by specifically binding to the binding cavity of a TNF-? homodimer. A composition containing the compound as well as uses of the compound and the composition in preventing or treating autoimmune diseases and/or inflammatory diseases are disclosed. Extracellular inactivation of TNF-? through protein-protein interface destruction is the most innovative and effective method for alleviating chronic systemic inflammatory states, and TIM series compounds, which have better efficacy and lower toxicity than those of existing TNF inhibitors and have oral bioavailability, can be effectively used as leading anti-inflammatory molecules.

Abstract: A peptide inhibiting a Toll-like receptor (TLR) signaling pathway is disclosed. The peptide strongly binds to a TIR-containing molecule to inhibit the TLR, in particular, the TLR4 signaling pathway. A fusion peptide in which a cell-penetrating peptide is conjugated to said peptide; a TLR4 antagonist comprising said peptide or said fusion peptide; and compositions and methods for preventing or treating autoimmune diseases or inflammatory diseases are disclosed. The peptide exhibits an inhibitory effect on a wide range of TLR signaling pathways including TLR4, blocks MyD88- and TRIF-dependent TLR4 pathways, and has a substantial disease-alleviating effect in mouse models of rheumatoid arthritis, psoriasis, systemic lupus erythematosus, and non-alcoholic steatohepatitis, and thus can be usefully utilized as therapeutics for immune-related diseases and inflammatory diseases that require negative control of TLR.

Abstract: The present invention relates to a fusion polypeptide that inhibits TLR1/2, TLR2/6, TLR7, TLR8 and TLR9 signaling pathways as well as Toll-like receptor 4 (TLR4) and TLR3, and a pharmaceutical composition for preventing or treating TLR pathway mediated diseases. The fusion peptide of the present invention has an excellent effect of inhibiting TLR4 and various TLR pathways and can be effectively used in preventing and treating various TLR pathway mediated diseases caused by the signaling pathways, such as autoimmune diseases, inflammatory diseases and degenerative neurological diseases, by inhibiting the TLR mediated immune responses.

Abstract: A substance P analog having a progenitor cell or stem cell recruiting activity and a method of recruiting progenitor cells or stem cells using the substance P analog are disclosed. The substance P analog has an effect of recruiting endogenous progenitor cells or stem cells to a wound or disease-occurring site. Thus, the disclosure also describes its use in recruiting progenitor cells or stem cells and a method of regenerating or treating a damaged organ or tissue, or a method of healing a wound.

Abstract: A substance P analog having a progenitor cell or stem cell recruiting activity and a method of recruiting progenitor cells or stem cells using the substance P analog are disclosed. The substance P analog has an effect of recruiting endogenous progenitor cells or stem cells to a wound or disease-occurring site. Thus, the disclosure also describes its use in recruiting progenitor cells or stem cells and a method of regenerating or treating a damaged organ or tissue, or a method of healing a wound.

Abstract: The present invention relates to a fusion polypeptide that inhibits TLR1/2, TLR2/6, TLR7, TLR8 and TLR9 signaling pathways as well as Toll-like receptor 4 (TLR4) and TLR3, and a pharmaceutical composition for preventing or treating TLR pathway mediated diseases. The fusion peptide of the present invention has an excellent effect of inhibiting TLR4 and various TLR pathways and can be effectively used in preventing and treating various TLR pathway mediated diseases caused by the signaling pathways, such as autoimmune diseases, inflammatory diseases and degenerative neurological diseases, by inhibiting the TLR mediated immune responses.

Abstract: The present disclosure relates to a novel small molecule TLR2 antagonist, and particularly, to 19 novel TLR2 antagonists, a pharmaceutical composition, including the antagonists, for preventing or treating inflammatory diseases, and a TLR4 regulator. The novel TLR2 antagonists according to the present disclosure can be effectively used as a preparation for oral administration by having low molecular weight and high oral bioavailability, and can be useful in pharmaceutical compositions for preventing or treating inflammatory diseases since the secretion of IL-8 is effectively inhibited and in vivo cytotoxicity is not induced. In addition, the novel TLR2 antagonists according to the present disclosure can be used as a TLR4 regulator.

Abstract: The present disclosure relates to a novel small molecule TLR2 antagonist, and particularly, to 19 novel TLR2 antagonists, a pharmaceutical composition, including the antagonists, for preventing or treating inflammatory diseases, and a TLR4 regulator. The novel TLR2 antagonists according to the present disclosure can be effectively used as a preparation for oral administration by having low molecular weight and high oral bioavailability, and can be useful in pharmaceutical compositions for preventing or treating inflammatory diseases since the secretion of IL-8 is effectively inhibited and in vivo cytotoxicity is not induced. In addition, the novel TLR2 antagonists according to the present disclosure can be used as a TLR4 regulator.

Abstract: The present disclosure relates to a peptide for inhibiting a TLR4 signaling pathway, a TLR4 antagonist including the peptide, and a composition for preventing or treating autoimmune diseases and inflammatory diseases. More specifically, the present disclosure relates to a peptide which binds to a TLR4/MD2 composite to inhibit the secretion of interleukin-6 (IL-6), NO, and ROS, and the activation of NF?B and MAPKs, a TLR4 antagonist including the peptide, and a composition for preventing or treating autoimmune diseases and inflammatory diseases. The peptide according to the present disclosure has an excellent effect of inhibiting the secretion of interleukin-6 (IL-6), NO, and ROS, and the activation of NF?B and MAPKs by inhibiting a TLR4 signaling pathway induced by a liphopolysaccharide (LPS), and thus can be favorably used as a composition for preventing or treating autoimmune diseases and inflammatory diseases occurring by the TLR4 signaling pathway.