a-2-ap

ADORA2A PDE4D-IN-1 (Compound 9) 是一种腺苷 A2a 受体（ADORA2A）和磷酸二酯酶 4D（PDE4D）的双重抑制剂，适用于支气管哮喘研究。

AP-1 NF-κB activation inhibitor 1 是一种有效的 AP-1和 NF-κB 介导的转录激活抑制剂(IC50=1 μM)，不阻断 β-actin 启动子驱动的基础转录。AP-1 NF-κB activation inhibitor 1 对受刺激细胞中 IL-2和 IL-8的产生水平有相似的抑制作用。

2-Hydroxybutyric acid (α-Hydroxybutyric acid) 是蛋白质代谢的产物，是 2 型糖尿病和先兆子痫的生物标志物，是合成生物降解材料和各种化合物的重要中间体。2-Hydroxybutyric acid 可预防 acetaminophen (AP) 引起的肝损伤，可参与抗肿瘤抗生素和可生物降解的聚（2-羟基丁酸）阿齐诺菊酯家族的合成。

BI-671800 (AP-761) 是高特异性的前列腺素 D2 受体拮抗剂，对哮喘有研究潜力，对人和小鼠 CRTH2 转染细胞中 PGD2 结合 CRTH2 的 IC50值分别为 4.5 和 3.7 nM。

SP-100030 是一种有效的 NF-κB 和激活蛋白-1 (AP-1) 双抑制剂 (IC50 分别为 50 和 50 nM)。SP-10003 抑制 Jurkat 和其他T 细胞系产生的 IL-2、IL-8 和 TNF-α 的产生。SP-100030 降低小鼠胶原性关节炎 (CIA)。

sEH inhibitor-16，作为一种可溶性环氧化物水解酶（sEH）抑制剂，具有2 nM的IC50值。它能够降低小鼠Cerulein诱导的急性胰腺炎（AP）的炎症损伤，适用于免疫炎症研究。

Benz-AP 是一种高效光敏剂，能产生单线态氧并与 hCES2 活性呈负相关。在 hCES2 低表达的癌细胞中，Benz-AP 表现出较高的光毒性。采用双光子激发(TPE)技术，Benz-AP 能够生成 ROS，有效杀死癌细胞和肿瘤球体。

Coenzyme Q0 (CoQ0)，一种从Antrodia cinnamomea提取的口服醌类化合物，具备促进细胞凋亡(apoptosis)与自噬(autophagy)的作用。该化合物通过抑制HER-2 AKT mTOR信号通路，增强凋亡和自噬机制；同时，调控NFκB AP-1活化，提升Nrf2稳定性，从而缓解炎症及氧化还原失衡。此外，Coenzyme Q0还表现出抗血管生成特性，通过下降MMP-9 NF-κB并提升HO-1信号路径发挥作用。

Kobophenol A has antimicrobial, and anti-inflammatory activities, it might be a candidate for treatment of inflammatory bone diseases relevant to osteoblast cell death. Kobophenol A inhibits AChE activity in a dose-dependent manner, and the IC50 value is

ADA-07 is a TOPK inhibitor which interacts with TOPK at the ATP-binding pocket and inhibits its kinase activity, thereby suppressing SUV-induced phosphorylation of ERK1 2, p38, and JNKs, and subsequently inhibiting AP-1 activity.

GYKI 52466 is an allosteric AMPA receptor antagonist. It selectively inhibits AMPA-induced inward currents (IC50 = 7.5 µM) over NMDA- or GABA-induced inward currents in primary rat hippocampal neurons at 50 µM but also inhibits kainate-induced inward currents in the same cells (IC50 = 11 µM).2 GYKI 52466 (10 µM) reduces the amplitude of spontaneous excitatory postsynaptic currents (EPSCs) in the same cells. It increases the latency to seizure onset and reduces mortality in a rat model of generalized tonic-clonic seizures induced by 4-aminopyridine (4-AP) when administered at doses of 25 and 50 mg kg. GYKI 52466 (30 mg kg) prevents neuronal damage in the CA1 region of the hippocampus in a rat model of global ischemia-reperfusion injury induced by four-vessel occlusion.

AP 811 acetate是一款选择性的ANP-CR（即NPR3）拮抗剂，其Ki值为0.48 nM。该化合物对NPR3的选择性是对NPR1的两万倍。此外，AP 811 acetate能够消除ANP诱导的泵激活现象。

Cafestol 是咖啡特有的一种二萜，可靶向 AP-1 抑制ERK，有化学预防、抗肿瘤、保肝、抗氧化和抗炎作用。它通过抑制NF-kB 活化途径强烈的抑制 PGE2的产生，还抑制 LGE 激活的 RAW264.7 细胞中的PGE2产生和环氧合酶(COX-2)的 mRNA 表达。

Antagonist G TFA 作为后叶加压素（vasopressin）的有效拮抗剂，同时对GRP和缓激肽具有弱拮抗作用。此外，Antagonist G 能够诱导AG-1转录，增强癌细胞对化疗的敏感性。

PAR-4 Agonist Peptide, amide TFA (PAR-4-AP (TFA)) 是一种蛋白酶激活受体 4 (PAR-4) 激动剂，对 PAR-1 或 PAR-2 均无影响，其作用可被 PAR-4 拮抗剂阻断。

FSL-1 TFA, a bacterial-derived toll-like receptor 2 6 (TLR2 6) agonist, enhances resistance to experimental HSV-2 infection[1]. FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB AP-1 signaling pathways in monocytic THP-1 cells[2]. FSL-1 significantly reduces HSV-2 replication in human vaginal epithelial cells (EC)[1].FSL-1 induces significant resistance to experimental genital HSV-2 infection through elaboration of a specific cytokine response profile[1].FSL-1 (50 ng mL, 24 hours) induces MMP-9 expression at both mRNA and protein levels in human monocytic THP-1 cells[2].FSL-1 activates the MAP kinase NF-κB signaling pathway[2]. Cell Viability Assay[1] Cell Line: V11I, V12I or V19I immortalized human vaginal EC FSL-1 application significantly protectes against genital HSV-2 challenge in mice[1]. Animal Model: Female Swiss-Webster mice (weighing 20-25 g)[1] [1]. William A Rose 2nd, et al. FSL-1, a bacterial-derived toll-like receptor 2 6 agonist, enhances resistance to experimental HSV-2 infection. Virol J. 2009 Nov 10;6:195. [2]. Cathryn J Kurkjian,et al. The Toll-Like Receptor 2 6 Agonist, FSL-1 Lipopeptide, Therapeutically Mitigates Acute Radiation Syndrome. Sci Rep. 2017 Dec 11;7(1):17355.