psd-95

Tramiprosate (Alzhemed) 是一种具有口服活性的、可透过血脑屏障的天然氨基酸，存在于各种红色海藻中，能够可溶性 Aβ 结合并以非原纤维形式维持 Aβ。它是一种 GABA 类似物，具有神经保护，抗惊厥和抗高血压的活性。

IC87201 是 PSD95-nNOS 相互作用的抑制剂，可抑制 nMDAR 诱导的一氧化氮和 cGMP 的形成，可用于缺血性中风和疼痛的研究。

Tat-NR2B9c (NA-1) 是一种突触后密度-95（PSD-95）抑制剂，具有神经保护和抗癫痫作用。Tat-NR2B9c 可抑制PSD-95d2、 PSD-95d1 和 PSD-95，可阻止NMDA诱导的神经元NADPH氧化酶的激活，从而阻断超氧化物的产生，可减少中风后急性期的缺血性损伤。

Tat-NR2B9c TFA is a 20-aa peptide, and acts as an inhibitor of postsynaptic density-95 (PSD-95)(EC50 of 6.7 nM for PSD-95d2), and possesses neuroprotective efficacy.

ZL006 是一种 nNOS PSD-95 相互作用抑制剂，能够抑制 NMDA 受体介导的 NO 合成。

Tat-NR2B9c acetate (NA-1 acetate) 是一种突触后密度 95 (PSD-95) 抑制剂，对 PSD-95d2 (PSD-95 PDZ domain 2) 和 PSD-95d1 的 EC50 值分别为 6.7 nM 和 670 nM。它破坏 PSD-95 NMDAR 相互作用，抑制 NR2A 和 NR2B 与 PSD-95 的结合，IC50 值分别为 0.5 μM 和 8 μM。它还抑制神经元一氧化氮合酶 (nNOS) PSD-95 相互作用，并具有神经保护功效。

SCR-4026 is an inhibitor of the nNOS-PSD-95 interaction with neuroprotective activities. SCR-4026 also promotes neural stem cells to differentiate into neurons-like cells.

Emodin-1-O-β-D-glucopyranoside (Emodin-1-O-glucoside) 是一种非竞争性细菌神经氨酸酶抑制剂，IC50为 0.85 μM，提取自药用植物虎杖中。

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.1 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.2 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.2,3,4,5,6 |1. Santos, M.J., López-Jurado, M., Llopis, J., et al. Influence of dietary supplementation with fish oil on plasma fatty acid composition in coronary heart disease patients. Ann. Nutr. Metab. 39(1), 52-62 (1995).|2. Lee, J.Y., Sohn, K.H., Rhee, S.H., et al. Saturated fatty acids, but not unsaturated fatty acids, induced the expression of cyclooxygenase-2 mediated through toll-like receptor 4. J. Biol. Chem. 276(20), 16683-16689 (2001).|3. Dietzen, D.J., Hastings, W.R., and Lublin, D.M. Caveolin is palmitoylated on multiple cysteine residues. Palmitoylation is not necessary for localization of caveolin to caveolae. J. Biol. Chem. 270(12), 6838-6842 (1995).|4. Robinson, L.J., and Michel, T. Mutagenesis of palmitoylation sites in endothelial nitric oxide synthase identifies a novel motif for dual acylation and subcellular targeting. Proc. Nat. Acad. Sci. USA 92(25), 11776-11780 (1995).|5. Topinka, J.R., and Bredt, D.S. N-terminal palmitoylation of PSD-95 regulates association with cell membranes and interaction with K+ channel Kv1.4. Neuron 20(1), 125-134 (1998).|6. Miggin, S.M., Lawler, O.A., and Kinsella, B.T. Palmitoylation of the human prostacyclin receptor. Functional implications of palmitoylation and isoprenylation. J. Biol. Chem. 278(9), 6947-6958 (2003).

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid-13C contains 13C at the C2 position and has been used in the study of free fatty acid incorporation into phospholipid fatty acids in soil microbes.1 Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.2 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.3 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.3,4,5,6,7

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].

Ethyl-3,4-dephostatin is a novel inhibitor of the interactions of CFTR-associated ligand and PSD-95 Dlg1 ZO-1 domain.

3,4-Dephostatin is an inhibitor of the interactions of CFTR-associated ligand (CAL) and PSD-95 Dlg1 ZO-1 (PDZ) domain.

PDZ1 Domain inhibitor peptide TFA，一种环状肽，以 β-Ala 内酰胺侧链为接头，专一性靶向 PSD-95 的 PDZ1 域。此化合物能干扰 GluR6 PSD-95 间的相互作用，通过与 GluR6 的 C 末端竞争，抑制其在 PDZ1 域的结合。

Tat-NR2BAA TFA 是 Tat-NR2B9c 的对照肽 (control peptide)，没有活性。Tat-NR2BAA TFA 的序列与 Tat-NR2B9c 相似，但在 COOH 末端 tSXV 基序中有一个双点突变，这使得它无法结合 PSD-95。Tat-NR2B9c TFA 是一种可通透细胞膜的多肽，破坏 PSD-95 NMDAR 的结合。

Novel cyclic peptide that disrupts interaction between GluR6 and PSD-95

AVLX-125 (UCCB01-125) 是 PSD-95 和 PDZ 结构域的抑制剂，Kd 值为 10 nM，适用于炎症性疼痛的研究。