ap-10

14-Deoxy-11,12-didehydroandrographolide (AP10) has hypotensive, anti-inflammatory, anti-asthma, and anti-cancer actions. It can inhibit NF-κB activation.

nociceptin/orphanin FQ (NOP) receptor antagonist

AP-102 is a bioactive chemical.

CAP-100 is a monoclonal antibody targeting CCR7. It neutralizes the ligand binding site and signaling of CCR7. This compound effectively inhibits migration, extravasation, homing, and survival in chronic lymphocytic leukemia (CLL) samples induced by CCR7. CAP-100 can mediate potent tumor cell killing through host immune mechanisms and exhibits favorable toxicity profiles in related hematopoietic cell subsets. It is involved in research on antitumor activity and diseases like chronic lymphocytic leukemia (CLL).

RAP-103 is an orally active CCR antagonist that effectively protects synapses by inhibiting and reversing cytoskeletal changes induced by PrPC/NOX signaling. RAP-103 is applicable for research in Alzheimer's disease (AD).

NAP1051, a biomimetic analog of Lipoxin A4, serves an anti-tumor role by targeting the inflammatory tumor microenvironment. It inhibits the chemotaxis of neutrophils to fMLP and stimulates macrophage efferocytosis by activating AKT. NAP1051 is utilized in research on colorectal cancer.

MRT-10 is a Smoothened (Smo) receptor antagonist.

Ketomethylenebestatin is a carba-analog of bestatin,the aminopeptidase (AP) inhibitor. Ketomethylenebestatin is 10 fold less effective as an inhibitor of aminopeptidases than bestatin.

Sulfaphenazole (Plisulfan) is an inhibitor of CYP2C9 (Ki: 0.3 μM) that demonstrates at least 100-fold selectivity over other CYP450 isoforms (Ki: 63/29 μM for CYP2C8/CYP2C18, respectively, and no activity at CYP1A1, CYP1A2, CYP3A4, CYP2C19). At 10 μM, sulfaphenazole has been shown to inhibit endothelium-derived hyperpolarizing factor synthase, a CYP450 isozyme in the porcine coronary artery homologous to CYP2C8/9 that generates reactive oxygen species in coronary endothelial cells and modulates vascular tone and homeostasis.

T-5224 is a selective inhibitor of the transcription factor c-Fos/activator protein (AP)-1 with anti-inflammatory effects. T-5224 specifically suppresses the DNA-binding activity of c-Fos/c-Jun, thereby inhibiting IL-1β-induced transcriptional upregulation of Mmp-3, Mmp-13, and Adamts-5, without affecting the binding activity of other transcription factors. T-5224 can be used in research on rheumatoid arthritis, osteoarthritis, and cartilage degeneration.

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-1, a miniaturized proteolysis-targeting chimera (PROTAC) incorporating an anaplastic lymphoma kinase (ALK) ligand connected to (±)-thalidomide via an ultrashort linker, effectively degrades ALK fusion proteins such as NPM-ALK in Karpas-299 cells and EML4-ALK and ALKF1174L in SN-N-SH and NCI H3122 cells, respectively. Concentrations ranging from 10 to 300 nM are sufficient for its action, which is hindered by the proteasome inhibitor MG-132. Demonstrating selectivity, AP-1 exhibits cytotoxicity towards ALK-dependent Karpas-299 cells with an IC50 value of 0.1265 nM, while showing significantly less toxicity to non-ALK-dependent THP-1 cells (IC50 = 2,704 nM). Furthermore, it effectively reduces tumor volume in NCI H3122 mouse xenograft models at doses of 25, 50, and 100 mg/kg.

Linoleoyl Ethanolamide is an endocannabinoid agent. It acts by binding to TRPV1 increasing ERK phosphorylation and AP-1 dependent transcription in CB-receptor in an independent manner.

Sulfaphenazole (Standard) is the standard substance of Sulfaphenazole, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Sulfaphenazole (Plisulfan) is an inhibitor of CYP2C9 (Ki: 0.3 μM) that demonstrates at least 100-fold selectivity over other CYP450 isoforms (Ki: 63/29 μM for CYP2C8/CYP2C18, respectively, and no activity at CYP1A1, CYP1A2, CYP3A4, CYP2C19). At 10 μM, sulfaphenazole has been shown to inhibit endothelium-derived hyperpolarizing factor synthase, a CYP450 isozyme in the porcine coronary artery homologous to CYP2C8/9 that generates reactive oxygen species in coronary endothelial cells and modulates vascular tone and homeostasis.

Antcin K is a selective inhibitor that targets the PI3K/Akt, NF-κB, MEK1/2-ERK, p38, and AP-1 pathways. It enhances IL-10 expression, thereby suppressing pro-inflammatory cytokine production, blocking monocyte adhesion, reducing tissue damage, and promoting myogenesis. Antcin K exhibits significant anti-inflammatory, anti-damage, and tissue-protective activities. It is primarily studied in the context of inflammatory-related diseases such as periodontitis, rheumatoid arthritis, and skeletal muscle injury.

Rocaglaol is a potent anticancer drug that induces apoptosis of LNCaP cells through the mitochondrial pathway and its G2/M-phase cell cycle arrest is associated with the down-regulation of Cdc25C and the dephosphorylation of Cdc2. Rocaglaol can reduce tis

ARP (Aldehyde reactive probe) is a chemical compound that serves as an aldehyde-reactive probe by specifically tagging AP sites in DNA with biotin residues. It is used to detect abasic sites, which are common forms of DNA damage and intermediates in mutagenesis and carcinogenesis. ARP is highly sensitive, capable of detecting abasic sites at the femtomolar level (fewer than 1 site per 10^4 nucleotides).