Alomone Labs is pleased to offer the NaV Channel Blockers for Pain Research Explorer Kit (#EK-375). The Explorer Kit contains NaV channel blockers for pain research, ideal for screening purposes.
|Product Name||Cat #||Size|
|A-105||1 x 10 mg|
|STH-100||1 x 0.1 mg|
|STH-102||1 x 50 µg|
|I-170||1 x 5 mg|
|N-310||1 x 5 mg|
|STP-400||1 x 50 µg|
|STP-100||1 x 50 µg|
|STT-100||1 x 0.1 mg|
|STT-150||1 x 50 µg|
|T-550||1 x 50 µg|
|STT-350||1 x 50 µg|
Voltage-dependent sodium channels (NaV) have functions in most electrically active cells and are vital for the propagation of action potentials in these cells. NaV channel inhibiting drugs have long been used as analgesic drugs with relatively mild side-effects and safe pharmacological profiles. The mechanism of analgesia by NaV channel blockage has been extensively studied.
Four NaV channel subtypes involved in pain are NaV1.3, 1.7, 1.8 and 1.9. NaV1.8 and 1.9 are referred to as tetrodotoxin (TTX)-resistant channels and are implicated in pain relief because action potentials in nociceptive neurons are characteristically also resistant to TTX. The relatively depolarized voltage-dependence of inactivation of NaV1.8 also allows these channels to contribute to action potential generation even at depolarized membrane potentials as may occur following nerve injury or pain signaling. Importantly, NaV1.8 was found to be almost exclusively localized to nociceptive DRG neurons – mainly in small diameter unmyelinated C-fibers, but also in some medium diameter, thinly myelinated Aδ-fibers. NaV1.9 channels are exclusively expressed in C-fibers. Studies suggest that it is responsible for the persistent component of TTX-r currents that are found in nociceptive DRG neurons, having very slow kinetics and a large window current due to a hyperpolarised voltage-dependence of activation compared to inactivation. NaV1.9 knockout mice have no neuropathic pain phenotype, but do show reduced hypersensitivity to inflammatory stimuli. NaV1.7 is also expressed in DRG cells, but unlike NaV1.8 and 1.9, it is sensitive to TTX and is expressed in both nociceptive and non-nociceptive peripheral neurons. NaV1.7 channels have unusually slow kinetics of open-state and closed-state inactivation, and these unusual gating properties may allow the channels to stay open during slow depolarizations, thus amplifying pain signals.
- Clare, J.J. (2010) Expert Opin. Investig. Drugs 19, 45.
- Anti-SCN3A (NaV1.3) Antibody (#ASC-004)
- Anti-SCN3A (NaV1.3) (extracellular) Antibody (#ASC-023)
- Anti-NaV1.7 (SCN9A) Antibody (#ASC-008)
- Anti-NaV1.7 (SCN9A)-ATTO Fluor-633 Antibody (#ASC-008-FR)
- Guinea pig Anti-NaV1.7 (SCN9A) Antibody (#ASC-008-GP)
- Anti-NaV1.7 (SCN9A) (extracellular) Antibody (#ASC-027)
- Anti-NaV1.8 (SCN10A) Antibody (#ASC-016)
- Anti-NaV1.8 (SCN10A)-ATTO Fluor-594 Antibody (#ASC-016-AR)
- Guinea pig Anti-NaV1.8 (SCN10A) Antibody (#ASC-016-GP)
- Anti-NaV1.8 (SCN10A) (extracellular) Antibody (#ASC-028)
- Anti-SCN11A (NaV1.9) Antibody (#ASC-017)
- Guinea pig Anti-SCN11A (NaV1.9) Antibody (#ASC-017-GP)
- NaV Channel Antibodies for Pain Research Explorer Kit (#AK-365)
- Classical Ion Channel Blockers for Pain Research Explorer Kit (#EK-355)
- Ion Channel Activators for Pain Research Explorer Kit (#EK-395)