a-2-ap

AP-1/NF-κB activation inhibitor 1 is a potent inhibitor of AP-1 and NF-κB mediated transcriptional activation ( IC 50 =1 μM), does not blocking basal transcription driven by the β-actin promoter. AP-1/NF-κB activation inhibitor 1 has a similar inhibitory effect on the production of IL-2 and IL-8 levels in stimulated cells [1].

BI-671800 (AP-761) is a highly specific and potent antagonist of chemoattractant receptor-homologous molecule on Th2 cells (DP2/CRTH2). With IC50 values of 4.5 nM and 3.7 nM for PGD2 binding to CRTH2 in hCRTH2 and mCRTH2 transfected cells, respectively. BI-671800 has the potential to treat poorly controlled asthma[2].

AP 811 acetate is a selective antagonist of the atrial natriuretic peptide clearance receptor (ANP-CR, NPR3), demonstrating high affinity with a K_i value of 0.48 nM and exhibiting over 20,000-fold selectivity for NPR3 compared to NPR1. It effectively inhibits ANP-induced pump stimulation [1] [2].

FSL-1 TFA, a toll-like receptor 2/6 (TLR2/6) agonist derived from bacteria, bolsters resistance against experimental HSV-2 infection[1] and stimulates MMP-9 production via the TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells[2].

sEH Inhibitor-16, a potent soluble epoxide hydrolase (sEH) inhibitor, exhibits an IC50 of 2 nM. It diminishes inflammatory damage associated with cerulein-induced acute pancreatitis (AP) in mice, making it suitable for inflammation and immunology research [1].

Coenzyme Q0 (CoQ0), a potent, orally active ubiquinone compound derived from Antrodia cinnamomea, induces apoptosis and autophagy. It suppresses HER-2/AKT/mTOR signaling, enhancing apoptosis and autophagy mechanisms. Additionally, Coenzyme Q0 regulates NFκB/AP-1 activation and promotes Nrf2 stabilization, contributing to the attenuation of inflammation and redox imbalance. It also exhibits anti-angiogenic activity by downregulating MMP-9/NF-κB and upregulating HO-1 signaling.

Benz-AP, a potent photosensitizer, generates singlet oxygen inversely related to Human carboxylesterase 2 (hCES2) activity, showcasing enhanced photocytotoxicity in cancer cells within low hCES2 environments. Moreover, upon Two-photon excitation (TPE), Benz-AP induces the production of reactive oxygen species (ROS), effectively killing cancer cells and tumor spheroids [1].

SP-100030 is a dual inhibitor of NF-κB and activator protein-1 (AP-1), demonstrating potent inhibition with IC50 values of 50 nM for both. It effectively reduces the production of IL-2, IL-8, and TNF-alpha in Jurkat and other T cell lines. Additionally, SP-100030 has been shown to decrease the severity of murine collagen-induced arthritis (CIA).

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.

15(S)-HpETE is a monohydroperoxy polyunsaturated fatty acid (PUFA) produced by the action of 15-lipoxygenase (15-LO) on arachidonic acid. It is either metabolized to 14,15-leukotriene A4 [1] or reduced to 15(S)-HETE by peroxidases.[2] [1] 15(S)-HpETE mediates a number of biological functions including the induction of c-fos and c-jun, and activation of AP-1. [3] 15(S)-HpETE inhibits prostacyclin synthesis in porcine aortic microsomes and bovine endothelial cells, and can cause the suicide inactivation of porcine 12-LO.[2][4][5]

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.

CAFESTOL is a ERK inhibitor for AP-1-targeted activity against PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 in LPS-activated RAW264.7 cells. Cafestol has strong inhibitory activity on PGE2 production by suppressing the NF-kB activation pathway.

Antagonist G TFA is a potent antagonist of vasopressin, with additional, weaker antagonistic effects on GRP and Bradykinin. This compound also promotes AP-1 transcription and enhances cellular sensitivity to chemotherapy [1] [2].

2-Hydroxybutyric acid (α-Hydroxybutyric acid) is a product of protein metabolism and a biomarker for type 2 diabetes and pre-eclampsia.

PAR-4 Agonist Peptide, amide TFA (PAR-4-AP (TFA)), is a selective activator of the proteinase-activated receptor-4 (PAR-4), demonstrating specificity by not influencing PAR-1 or PAR-2, and its activity can be inhibited by a PAR-4 antagonist.