cav3.1

SAK3 is a novel modulator of nAChR activity that enhances T-type voltage-gated Ca2+ channel (T-VGCC) activity, and has potentiating effects on both Cav3.1 and Cav3.3 T-type Ca2+ channel currents.SAK3 is neuroprotective against scopolamine-induced cholinergic dysfunction in human neuroblastoma SH-SY5Y cells.SAK3 is used for the study of memory deficits and Alzheimer's disease. SAK3 can be used to study memory deficits and Alzheimer's disease.

ML218 hydrochloride is a selective and orally active T-type Ca2+ channels (Cav3.1, Cav3.2, Cav3.3) inhibitor (Cav3.2 and Cav3.3 with IC50s of 310 nM and 270 nM , respectively).

ML218 is an orally active, selective, potent, and blood-brain barrier-crossing inhibitor of T-type Ca2+ channels (Cav3.1, Cav3.2, Cav3.3) (IC50 for Cav3.2 and Cav3.3 is 310 nM and 270 nM, respectively).ML218 inhibits the burst activity of neurons in the subthalamic nucleus (STN).

Apinocaltamide (ACT-709478) is an orally available and selective T-type calcium channel blocker that penetrates the blood-brain barrier (BBB) with IC50=6.4-18nM for Cav3.1, Cav3.2, and Cav3.3, and is commonly used in epilepsy research.

Cav 3.1 blocker 1 (compound 12) is a T-type calcium channel inhibitor with an IC50 value of 160 nM for Cav3.1. It exhibits weaker inhibition on Cav 3.2 with an IC50 of 5000 nM and shows no inhibitory effect on Cav 3.3 and Cav 1.2 (IC50 > 10000 nM).

5(6)-EET is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5(6)-EET degrades into 5,6-DiHET and 5(6)-δ-lactone, which can be converted to 5(6)-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5(6)-EET has been implicated in the mobilization of calcium and hormone secretion. 5(6)-EET is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC50 = 0.54 μM), and Cav3.3 and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 μM. (±)5(6)-EET is provided as a mixture of the free acid and lactone.

TTA-P2 (T-Type calcium channel inhibitor) is a potent inhibitor of T-type calcium channels. It effectively penetrates the CNS and blocks natural T-type currents in deep cerebellar nucleus neurons, completely eliminating window currents in wild-type and mutant Cav3.1 channels. [research]

T-Type calcium channel inhibitor 2 (compound 6g) is a potent inhibitor of the T-type calcium channel, specifically acting on Cav3.1 (α1G) with an IC50 of 31.0 μM, Cav3.2 (α1H) with an IC50 of 83.1 μM, and Cav3.3 (α1I) (α1H). T-Type calcium channel inhibitor 2 exhibited cytotoxicity against A549 and HCT-116 cells with IC50s of 5.0 μM and 6.4 μM, respectively.

GTx1-15, an inhibitor cystine knot (ICK) peptide, antagonizes the voltage-dependent calcium channel Cav3.1, as well as voltage-dependent sodium channels Nav1.3 and Nav1.7 [1].

Kurtoxin is a selective Cav3 (T-type) voltage-gated Ca2+ channel gating inhibitor with a dissociation constant (Kd) of 15 nM for the Cav3.1 (α1G T-type) Ca2+ channel. It exhibits high-affinity interactions with native neuronal high-threshold L-type, N-type, and P-type Ca2+ channels in both central and peripheral neurons and displays cross-reactivity with the voltage-gated Na+ channel [1].

TTA-A2 is a selective T-type calcium channel antagonist as a potent anticonvulsant that the Cav3.1 isoform plays a prominent role in mediating. TTA-A2 is equally potent against the Cav3.1 (a1G) and Cav3.2 (a1H) channels with IC50 values of 89 nM and 92 nM, respectively, at -80 and -100 mV holding potentials. TTA-A2 can be used for the research of a variety of human neurological diseases, including sleep disorders and epilepsy.

Selective CaV3.1 channel blocker (IC50 values are 0.2 and 31.8 μM for hCaV3.1 and hCaV3.2 respectively). Also reversibly inhibits NaV1.8 and blocks KV2.1 channels.