Tr-PEG2-OH is a PEG-based PROTAC linker utilized in PROTAC synthesis[1]. It also serves as a non-cleavable 2-unit PEG ADC linker for the synthesis of antibody-drug conjugates (ADCs)[2].
TRβ agonist 2 (Compound 1) is a highly potent agonist of TRβ. Moreover, it effectively reduces lipid accumulation in HepG2 cells and promotes lipolysis, offering comparable effects. With its promising attributes, TRβ agonist 2 emerges as a potential thyromimetics that selectively targets TRβ [1].
Protein conjugates in tissue regeneration 2 (PCTR2) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid . DHA is oxidized to 16S,17S-epoxy-protectin, which is converted to PCTR1 by glutathione S-transferase and to PCTR2 via γ-glutamyl transpeptidase. PCTR2 is found in resolving mouse exudate and in both M1 and M2 macrophages differentiated from isolated human monocytes.
Levocarbastine is a second-generation H1 receptor antagonist for allergic conjunctivitis. It also acts as a potent selective antagonist for the neurotensin receptor NTS2 and is the first drug to be used to characterize different neurotensin subtypes.
Maresin conjugates in tissue regeneration 2 (MCTR2) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase then to MCTR2 by γ-glutamyl transferase. MCTR2 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR2 prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR2 selectively reduced the amount of the eicosanoids PGD2 and PGF2α in the exudate.