Dimethandrolone (DMA), also known by its developmental code name CDB-1321, is an experimental androgen anabolic steroid (AAS) and progestogen medication which is under investigation for potential clinical use. Dimethandrolone is an AAS, and hence is an agonist of the androgen receptor, the biological target of androgens like testosterone. It is also a progestin, or a synthetic progestogen, and hence is an agonist of the progesterone receptor, the biological target of progestogens like progesterone.
Handle region peptide, rat, functions as a prorenin receptor antagonist, effectively inhibiting the development of diabetic nephropathy while also exhibiting anti-inflammatory properties specifically within the eye.
Thiorphan disulfide is an impurity of Racecadotril -- an antidiarrheal and enkephalinase inhibitor that reduces the amount of water and electrolytes absorbed into the intestine.
Tat-NR2BAA is an inactive control peptide of Tat-NR2B9c. It shares a similar sequence with Tat-NR2B9c, but possesses a double-point mutation in the COOH terminal tSXV motif. This mutation renders Tat-NR2BAA unable to bind PSD-95. Tat-NR2B9c, on the other hand, is a membrane-permeable peptide that interferes with PSD-95 NMDAR binding. This interference leads to the decoupling of NR2B- and or NR2A-type NMDARs from PSD-95[1][2].
ABO acts as an annexin A7 modulator, specifically binding to Thr286 to inhibit its phosphorylation on threonine (not on serine or tyrosine) residues within human umbilical vein endothelial cells (HUVECs). This compound furthers the annexin A7 interaction with the EF-hand protein GCA, leading to reduced GCA phosphorylation, lowered intracellular calcium levels, and enhanced autophagy in COS-7 cells. Moreover, ABO lessens phosphorylation of the microtubule-associated protein 1 light chain (LC3) in HUVECs and impedes the upregulation of phosphatidylcholine-specific phospholipase C (PC-PLC) due to oxidized low-density lipoprotein in vascular endothelial cells (VECs). In animal models, specifically apoE-/- mice on a Western diet, administration of ABO (50 or 100 mg/kg per day) has been shown to decrease PC-PLC expression, promote autophagy, and reduce apoptosis, lipid accumulation, and the extent of atherosclerotic plaques in the aortic endothelium.