GYKI 52466 dihydrochloride is a potent, selective, orally active and non-competitive kainate- and AMPA-activated currents antagonist with IC50s of 7.5 μM and 11 μM, respectively. GYKI 52466 dihydrochloride is inactive against N-methyl-D-aspartate (NMDA) or γ-aminobutyric acid responses. GYKI 52466 dihydrochloride ia a muscle relaxant and anticonvulsant agent, and has good blood brain barrier permeability[1][2].
Clobutinol hydrochloride is a compound that has anti-tussive effects. Clobutinol hydrochloride affects heart rate and blood pressure, it can be used for cough related research[1][2][3].
A 803467 is a selective Nav1.8 sodium channel blocker with an IC50 of 8 nM; over 100-fold more selective vs. human Nav1.2, 1.3, 1.5 and 1.7. IC50 value: 8 nMTarget: Nav1.8 sodium channelA 803467 dose-dependently reduces behavioral responses in a variety of neuropathic and inflammatory pain models.
L-Glutamic acid-13C5,15N is the 13C- and 15N-labeled L-Glutamic acid. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
PAC-14028 is a potent and selective transient receptor potential vanilloid type I (TRPV1) antagonist.
Phenibut (β-Phenyl-GABA) hydrochloride is an orally active GABA-B agonist[1]. Phenibut hydrochloride acts as a GABA-mimetic, primarily at GABAB receptors. Phenibut hydrochloride has anxiolytic and nootropic (cognition enhancing) effects[2].
Ranolazine is an antianginal medication.Target: Sodium ChannelRanolazine is believed to have its effects via altering the transcellular late sodium current. It affects the sodium-dependent calcium channels during myocardial ischemia in rabbits by altering the intracellular sodium level [1]. Thus, ranolazine indirectly prevents the calcium overload that causes cardiac ischemia in rats [2]. The effects of ranolazine on the NaV 1.7 and NaV 1.8 sodium channels also make it potentially useful in the treatment of neuropathic pain. Ranolazine produced dose-dependant analgesia on mechanical allodynia induced by CFA injection, but had no effect on thermal hyperalgesia [3, 4].
Selurampanel (BGG 492) is an orally active and competitive AMPA receptor antagonist with an IC50 of 190 nM. Selurampanel has reasonable blood-brain barrier penetration. Selurampanel can be used for epilepsy research[1][2].
(S)-Willardiine is a potent agonist of AMPA/kainate receptors with EC50 of 44.8 uM.IC50 value: 44.8 uM(EC50) [1]Target: AMPA/kainate receptor agonistin vitro: The (S)- but not (R)-isomers of willardiine and 5-bromowillardiine were potent agonists, producing rapidly but incompletely desensitizing responses [1]. At a concentration of 1.8 mM, Ca2+ inhibited the currents induced by 100 microM willardiine by approximately 50% [2].in vivo: In newborn mice (P5, histopathology at P10), local injection of the AMPA receptor agonist S-bromo-willardiine at day 5 after birth induced cortical damage and white matter damage, which was reduced in a dose-dependent manner by the AMPA receptor antagonists [3].
IK1 inhibitor PA-6 (PA-6), a pentamidine analogue, is a selective and potent IK1 (KIR2.x ion-channel-carried inward rectifier current) inhibitor, with IC50 values of 12-15 nM for human and mouse KIR2.x currents. IK1 inhibitor PA-6 (PA-6) elevates KIR2.1 protein expression and induces intracellular KIR2.1 accumulation. IK1 inhibitor PA-6 (PA-6) has the potential to treat atrial fibrillation and arrhythmia[1][2][3].
BAY-1797 is a potent, orally active, and selective P2X4 antagonist, with an IC50 of 211 nM against human P2X4. BAY-1797 displays no or very weak activity on the other P2X ion channels. BAY-1797 shows anti-nociceptive and anti-inflammatory effects[1].
BI 01383298 is a potent inhibitor of the sodium-citrate co-transporter (SLC13A5) that is highly expressed in the liver[1].
YHO-13351 (free base) is the water-soluble prodrug of YHO-13177, which is a potent and specific inhibitor of BCRP.IC50 value:Target: BCRP inhibitorin vitro: YHO-13177 potentiates the cytotoxicity of SN-38, mitoxantrone, and topotecan in both BCRP-transduced human colon cancer HCT116 (HCT116/BCRP) cells and SN-38-resistant human lung cancer A549 (A549/SN4) cells that express BCRP, but had little effect in the parental cells. In addition, YHO-13177 potentiates the cytotoxicity of SN-38 in human lung cancer NCI-H460 and NCI-H23, myeloma RPMI-8226, and pancreatic cancer AsPC-1 cells that intrinsically expressed BCRP. YHO-13177 increases the intracellular accumulation of Hoechst 33342, a substrate of BCRP, at 30 minutes and partially suppresses the expression of BCRP protein at more than 24 hours after its treatment in both HCT116/BCRP and A549/SN4 cells [1].in vivo: In mice, YHO-13351 is rapidly converted into YHO-13177 after its oral or intravenous administration. Coadministration of irinotecan with YHO-13351 significantly increases the survival time of mice inoculated with BCRP-transduced murine leukemia P388 cells and suppressed the tumor growth in an HCT116/BCRP xenograft model, whereas irinotecan alone has little effect in these tumor models [1].
Niflumic acid, a Ca2+-activated Cl- channel blocker, is an analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.Target: Othersniflumic acid, an inhibitor of calcium-activated chloride currents. Niflumic acid does not block directly calcium channels or activate potassium channels. Niflumic acid selectively reduces a component of noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels [1]. Niflumic acid molecule is completely buried in the substrate-binding hydrophobic channel. The conformations of the binding site in PLA(2) as well as that of niflumic acid are not altered upon binding [2]. Niflumic acid (NFA) produces biphasic behavior on human CLC-K channels that suggests the presence of two functionally different binding sites: an activating site and a blocking site [3].
Propafenone (SA-79), a sodium-channel blocker, acts an antiarrhythmic agent. Propafenone also has high affinity for the β receptor (IC50=32 nM)[1]. Propafenone blocks the transient outward current (Ito) and the sustained delayed rectifier K current (Isus) with IC50 values of 4.9 μm and 8.6 μm, respectively[2]. Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction and induce apoptosis[3].
IC87201, an inhibitor of PSD95-nNOS protein-protein interactions, suppresses NMDAR-dependent NO and cGMP formation.
NS8593 hydrochloride is a potent and selective small conductance Ca2+-activated K+ channels (SK channels) inhibitor. NS8593 hydrochloride reversibly inhibits SK3-mediated currents with a Kd value of 77 nM. NS8593 hydrochloride inhibits all the SK1-3 subtypes Ca2+-dependently (Kds of 0.42, 0.60, and 0.73 μM, respectively, at 0.5 μM Ca2+), and does not affect the Ca2+-activated K+ channels of intermediate and large conductance (hIK and hBK channels, respectively)[1][2].
Org 26576 is a AMPA receptor positive allosteric modulator.
ASIC-IN-1 is a potent acid sensing ion channel inhibitor with an IC50 value of < 10 µM. ASIC-IN-1 causes a dose- dependent reduction of the pain intensity[1].
Opiranserin (VVZ-149) hydrochloride, a non-opioid and non-NSAID analgesic candidate, is a dual antagonist of glycine transporter type 2 (GlyT2) and serotonin receptor 2A (5HT2A), with IC50s of 0.86 and 1.3 μM, respectively. Opiranserin hydrochloride shows antagonistic activity on rP2X3 (IC50=0.87 μM). Opiranserin hydrochloride is development as an injectable agent for the treatment of postoperative pain[1][2][3].
Annonacin is an Acetogenin and promotes cytotoxicity via a pathway inhibiting the mitochondrial complex. Annonacin is the active agent found in Graviola leaf extract to act as an inhibitor of sodium/potassium (NKA) and sarcoplasmic reticulum (SERCA) ATPase pumps[1].
Chembridge-5861528 is a TRPA1 channel blocker that antagonizes AITC- and 4-HNE-evoked calcium influx (IC50 values are 14.3 and 18.7μM respectively).
Indole-2-carboxylic acid is a strong inhibitor of lipid peroxidation. Indole-2-carboxylic acid (I2CA) specifically and competitively inhibits the potentiation by glycine of NMDA-gated current[1][2].
PF-06305591 is a potent and highly selective voltage gated sodium channel NaV1.8 blocker, with an IC50 of 15 nM. An excellent preclinical in vitro ADME and safety profile[1].
Guanosine 5'-diphosphate (GDP) sodium is a nucleoside diphosphate that activates adenosine 5'-triphosphate-sensitive K + channel. Guanosine 5'-diphosphate sodium is a potential iron mobilizer, which prevents the hepcidin-ferroportin interaction and modulates the interleukin-6 (IL-6)/stat-3 pathway. Guanosine 5'-diphosphate sodium can be used in the research of inflammation, such as anemia of inflammation (AI)[1][2].
Anthracene-9-carboxylic acid-d9 is the deuterium labeled Anthracene-9-carboxylic acid[1]. Anthracene-9-carboxylic acid (9-Anthracenecarboxylic acid) is an anthracene derivative traditionally used to block and identify Ca2+-activated Cl- currents (CaCCs) in various cell types, like diverse smooth muscle cells, epithelial cells and salivary gland cells[2].
PF 05089771 is a Nav1.7 channel blocker extracted from patent WO/2010/079443 A1, compound example 788, has an IC50 of 8.6 nM.
Maurocalcine is an agonist of ryanodine receptor (RyR) channel types 1, 2 and 3 with cellular permeability. Maurocalcine induces [3H]ryanodine binding on RyR1 with an EC50 value of 2558 nM. Maurocalcine exhibits a apparent affinity of 14 nM for RyR2. Maurocalcine can be applied to in vivo cell tracking or other cell imaging techniques[1][2][3].
Flunarizine is a potent dual Na+/Ca2+ channel (T-type) blocker. Flunarizine is a D2 dopamine receptor antagonist. Flunarizine shows anticonvulsive and antimigraine activity, and peripheral vasodilator effects[1][2][3][4][5].
SM-6586 is a calcium channel antagonist and inhibitor of Na+/H+ and Na+/Ca2+ exchange transport, potentially for the treatment of cerebrovasular diseases and hypertension.