This product is freeze dried. All water molecules have been removed.
Every lot is tried & tested in a relevant biological assay.
- Liu, G. et al. (2003) Neuropharmacology 44, 413.
- Alomone Labs Lamotrigineblocks NaV1.2 channels expressed in Xenopus oocytes.A. Time course of NaV1.2 current amplitude and inhibition by 100 and 300 µM Lamotrigine (#L-205). Currents were elicited by application of a 100 ms voltage step to 0 mV (H.P= -50 mV, to induce inactivation), every 10 seconds. B. Superimposed example traces of current responses before and during perfusion of 100 and 300 µM Lamotrigine, as indicated.
Voltage-gated sodium (NaV) channels contribute to physiological and pathophysiological electrical signaling in nerve and muscle cells. The channels play a role in the generation and propagation of action-potential in excitable cells. Eukaryotic NaV channels are heteromeric membrane proteins composed of a pore-forming α-subunit and auxiliary β-subunits1.
Lamotrigine (Lamictal) is a selective blocker of NaV1.2 channels with an IC50 of ≈70-140 μM for NaV1.22. Lamotrigine’s KD value for inactivated-state block of rat brain NaV1.2 expressed in Xenopus oocytes is 31.9 μM. High affinity blocking of sodium channels by Lamotrigine requires sustained membrane depolarization thus suggesting a higher affinity of the drug to Na+ channels in their inactive state. Sodium channels with a mutation in the transmembrane segment IVS6 have reduced affinity for blocking by Lamotrigine3. Lamotrigine is widely used as an anti-epileptic drug in different types of epilepsy. Unlike other Anti-epileptic drugs (AED), Lamotrigine does not decrease endogenous estrogen and progesterone production. In addition, Lamotrigine does not alter testosterone levels in women but mildly reduces androstenedione and mildly increases DHEA levels4. Lamotrigine causes fewer adverse effects than other drugs of its kind in patients with partial epilepsy5.
Lamotrigine (#L-205) is a highly pure, synthetic, and biologically active compound.
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