ap 4

L-APB is an effective and specific agonist for the group III mGluRs (EC50s: 0.13, 0.29, 1.0, 249 μM for mGlu4, mGlu8, mGlu6, and mGlu7 receptors, respectively).

broad spectrum excitatory amino acid receptor antagonist

Group III mGlu receptor agonist

L-AP4 (L-APB) monohydrate is a potent and specific agonist for group III mGluRs, with EC50s of 0.13, 0.29, 1.0, and 249 μM for mGlu4, mGlu8, mGlu6, and mGlu7 receptors, respectively [1][2].

DL-AP4, also known as 2-Amino-4-phosphonobutyric acid, is a competitive glutamate antagonist with defined binding affinity that is widely used to selectively inhibit glutamatergic neurotransmission, making it an essential experimental compound for probing synaptic signaling mechanisms and functional circuitry in central nervous system and visual system research.

AP-4 is an antagonist of the NMDA glutamate receptor.

Broad spectrum EAA ligand

AP-4-139B is a potent inhibitor of Heat Shock Protein 70 (HSP70), with an IC50 value of 180 nM. HSP70 is a protein that is overexpressed in various cancers and plays a critical role in the survival and proliferation of tumor cells. AP-4-139B demonstrates significant cytotoxicity in tumor cells, particularly in colorectal cancer cells, making it useful for cancer research.

MSOP is a selective antagonist of group III metabotropic glutamate receptor (KD of 51 μM for the L-AP4-sensitive presynaptic mGluR).

Ap4dT serves as an inhibitor of human adenylate kinase isozyme 1 (hAK1), effectively suppressing the synthesis of ATP and ADP, with IC50 values of 42 μM and 38 μM, respectively.

Ap4A (1, 10 µM; 24 h) induces apoptosis in HL60 cells.

Ap4G, a dinucleotide polyphosphate compound, possesses vasoconstrictive activity and regulates vascular constriction via the P2 receptors, particularly the P2X receptors. It serves as a vital tool for researching vascular physiology and pathology.

Ap4C tetrasodium is a dinucleotide polyphosphate that includes both purine and pyrimidine bases. This compound functions as a signaling molecule by interacting with specific P2Y receptors. It activates P2Y2 and P2Y4 receptors in platelets, inducing platelet aggregation and other cellular responses. Ap4C tetrasodium is utilized in studies related to inflammation and blood coagulation.

Ap4A tetraammonium, a conserved second messenger across organisms from bacteria to humans, binds and activates the transcription of MITF downstream genes in conjunction with histidine triad nucleotide-binding protein 1 (HINT1). Additionally, Ap4A tetraammonium induces cell apoptosis (apoptosis).

AP-III-a4 (ENOblock) (ENOblock) is the first nonsubstrate analogue inhibitor of enolase with IC50 of 0.576 μM.

AP-III-a4 hydrochloride (ENOblock hydrochloride) is a direct enolase (enolase) inhibitor with non-substrate analogs.AP-III-a4 hydrochloride inhibits metastasis of cancer cells in vivo and affects glucose homeostasis and can be used in bioassays.

Ortho-methyl 4-AP-1-ethyl Carbamate is used as a precursor for the synthesis of ortho-methylfentanyl.

voltage-dependent K+ channel blocker

AP-C4 is a selective inhibitor targeting guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII), exhibiting a pIC50 value of 5.2. Conversely, AP-C3 does not inhibit cGKII-mediated anion secretion [1].

5Me3F4AP is an effective potassium channel blocker, with an IC50 ranging from 220 μM to 693 μM as the pH increases from 6.4 to 9.1. It has the potential to cross the blood-brain barrier and may be used in positron emission tomography (PET).

TAK1/MAP4K2 inhibitor 1 (compound 5) is a dual kinase inhibitor of TAK1 and MAP4K2 with IC50 values of 41.1 nM and 18.2 nM, respectively.

GNE-1858 is an ATP-competitive hematopoietic progenitor kinase-1 (HPK1) inhibitor (IC50s of 1.9 nM, 1.9 nM, and 4.5 nM for wild-type and the active mimetic mutants HPK1-TSEE and HPK1-SA).

Ketoprofen (RP-19583) is a propionic acid derivative and nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic effects. It inhibits cyclo-oxygenase I and II, decreasing the formation of prostaglandin and thromboxane precursors. This reduction in prostaglandin synthesis, mediated by prostaglandin synthase, is responsible for its therapeutic effects. Additionally, Ketoprofen decreases thromboxane A2 formation via thromboxane synthase, inhibiting platelet aggregation.

GNE-220 is a potent and selective inhibitor of MAP4K4, with an IC50 of 7 nM.