1. Membrane Transporter/Ion Channel
  2. Potassium Channel
  3. AmmTX3 TFA

AmmTX3 TFA is a peptide toxin identified from the venom of the scorpion Androctonus mauretanicus. AmmTX3 TFA is a highly specific blocker of Kv4 channels, which selectively and almost completely blocks transient A-type K+ currents with a Ki of 131 nM. AmmTX3 TFA induces epileptiform behaviors and causes death in mice receiving intracerebroventricular injection. AmmTX3 TFA increases the excitability of dentate gyrus granule cells, reduces GABAergic inhibition, enhances and stabilizes the EPSP-spike component of long-term potentiation, and impairs reference memory. AmmTX3 TFA can be used in research related to pain, epilepsy, and autism spectrum disorder.

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AmmTX3 TFA

AmmTX3 TFA Chemical Structure

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Description

AmmTX3 TFA is a peptide toxin identified from the venom of the scorpion Androctonus mauretanicus. AmmTX3 TFA is a highly specific blocker of Kv4 channels, which selectively and almost completely blocks transient A-type K+ currents with a Ki of 131 nM. AmmTX3 TFA induces epileptiform behaviors and causes death in mice receiving intracerebroventricular injection. AmmTX3 TFA increases the excitability of dentate gyrus granule cells, reduces GABAergic inhibition, enhances and stabilizes the EPSP-spike component of long-term potentiation, and impairs reference memory. AmmTX3 TFA can be used in research related to pain, epilepsy, and autism spectrum disorder[1][2][3].

In Vitro

AmmTX3 (1 h) TFA binds with high affinity to a specific site on rat brain synaptosomes, fully displacing 125I-labelled sBmTX3 with a Ki of 19.5 pM, and exhibits a Kd of 66 pM for its own binding site[1].
AmmTX3 (0.1 nM-10 μM) TFA potently blocks the A-type K+ current in primary striatal neurons in culture, with a Ki of 131 nM, and its inhibitory effect is reversible[1].
AmmTX3 (0.5 μM) TFA potently blocks Kv4.2 channel currents in CHO-K1 cells co-expressed with DPP6S (with or without KChIP1), but only weakly blocks Kv4.2 + KChIP1 currents, demonstrating DPP6S confers high AmmTX3 TFA sensitivity to Kv4.2 channels[3].
AmmTX3 (0.5 μM) TFA potently blocks Kv4.3 channel currents in CHO-K1 cells co-expressed with DPP10a, but only weakly blocks Kv4.3 + KChIP1 currents, demonstrating DPP10a confers high AmmTX3 TFA sensitivity to Kv4.3 channels[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

AmmTX3 (0.75 mg; i.c.v.; single injection) TFA impairs spatial reference memory consolidation when administered during early stages of eight-arm radial maze training, causing a 1-day learning delay when injected after session 1 and increasing reference memory errors in session 4 when injected after session 3, with no effect on working memory[2].
AmmTX3 (0.75 mg; i.c.v.; single injection) TFA increases and stabilizes the EPSP-spike component of long-term potentiation in the dentate gyrus from 90 minutes post-high-frequency stimulation, with no effect on basal synaptic transmission or short-term plasticity[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague Dawley (male, 280-400 g)[2]
Dosage: 0.75 mg
Administration: i.c.v.; single injection
Result: Showed no significant differences in reference or working memory errors when injected 30 minutes before session 2.
Significantly increased reference memory errors in sessions 2 and 3, delayed learning by 1 day, and significantly increased total turns and 45° turns in sessions 2, 3, and 4 when injected immediately after session 1.
Significantly increased reference memory errors in session 4 when injected immediately after session 3.
Showed no significant differences in reference or working memory errors when injected immediately after session 5.
Animal Model: Sprague Dawley (male, 280-400 g)[2]
Dosage: 0.75 mg
Administration: i.c.v.; single injection
Result: Showed no significant differences in basal transmission (input-output curves, baseline field EPSP slope, population spike amplitude) or short-term plasticity (paired-pulse ratio) compared to vehicle group.
Increased field EPSP slope by 16.1% post-stimulation, remaining above baseline for 30 minutes, with no significant difference from vehicle group at any post-stimulation time point.
Maintained population spike amplitude above baseline for the full 4-hour recording period, while vehicle group's amplitude steadily decreased; significant difference between groups emerged 90 minutes post-induction.
Molecular Weight

3822.47 (free acid)

Formula

C158H262N50O48S6.xC2HF3O2

Sequence

{Glp}-Ile-Glu-Thr-Asn-Lys-Lys-Cys-Gln-Gly-Gly-Ser-Cys-Ala-Ser-Val-Cys-Arg-Lys-Val-Ile-Gly-Val-Ala-Ala-Gly-Lys-Cys-Ile-Asn-Gly-Arg-Cys-Val-Cys-Tyr-Pro (Disulfide bonds: Cys8-Cys28, Cys13-Cys33, Cys17-Cys35) (TFA salt)

Sequence Shortening

{Glp}-IETNKKCQGGSCASVCRKVIGVAAGKCINGRCVCYP (Disulfide bonds: Cys8-Cys28, Cys13-Cys33, Cys17-Cys35) (TFA salt)

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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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AmmTX3 TFA
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HY-P1426A
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