Size: | Price | Quantity | |
---|---|---|---|
5 mg | $75.00 | ||
25 mg | $275.00 |
ZJ43 (723331-20-2) is potent inhibitor of glutamate carboxypeptidases II (Ki = 0.8 nM) and III (Ki = 23 nM).1 It potently (IC50 = 2.4 nM) inhibited the ability of glutamate carboxypeptidase II to hydrolyze the neurotransmitter N-acetylaspartylglutamate (NAAG) resulting in an increase in synaptic levels of group II mGluRs. Peripherally administered ZJ43 increased the activation of mGluR3 by NAAG released from peripheral sensory neurites resulting in analgesia.2,3 ZJ43 has also shown efficacy in other inflammatory pain models.4,5
References/Citations:
1) Olszewski et al. (2004), NAAG peptidase inhibition reduces locomotor activity and some stereotypes in the PCP model of schizophrenia via group II mGluR; J. Neurochem. 89 876
2) Yamamoto et al. (2004), Antinociceptive effects of N-acetylaspartylglutamate (NAAG) peptidase inhibitors ZJ-11, ZJ-17 and ZJ-43 in the rat formalin test and in the rat neuropathic pain model; Eur. J. Neurosci. 20 483
3) Yamamoto et al. (2007), Local administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in peripheral pain in rats; Eur. J. Neurosci. 25 147
4) Yamamoto et al. (2008), Intracerebroventricular administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in inflammatory pain; Mol. Pain 4 31
5) Nonaka et al. (2017), A role for the locus coeruleus in the analgesic efficacy of N-acetylaspartylglutamate peptidase (GCPII) inhibitors ZJ43 and 2-PMPA; Mol.Pain 13 1
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ZJ43 (723331-20-2) is potent inhibitor of glutamate carboxypeptidases II (Ki = 0.8 nM) and III (Ki = 23 nM).1 It potently (IC50 = 2.4 nM) inhibited the ability of glutamate carboxypeptidase II to hydrolyze the neurotransmitter N-acetylaspartylglutamate (NAAG) resulting in an increase in synaptic levels of group II mGluRs. Peripherally administered ZJ43 increased the activation of mGluR3 by NAAG released from peripheral sensory neurites resulting in analgesia.2,3 ZJ43 has also shown efficacy in other inflammatory pain models.4,5
References/Citations:
1) Olszewski et al. (2004), NAAG peptidase inhibition reduces locomotor activity and some stereotypes in the PCP model of schizophrenia via group II mGluR; J. Neurochem. 89 876
2) Yamamoto et al. (2004), Antinociceptive effects of N-acetylaspartylglutamate (NAAG) peptidase inhibitors ZJ-11, ZJ-17 and ZJ-43 in the rat formalin test and in the rat neuropathic pain model; Eur. J. Neurosci. 20 483
3) Yamamoto et al. (2007), Local administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in peripheral pain in rats; Eur. J. Neurosci. 25 147
4) Yamamoto et al. (2008), Intracerebroventricular administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in inflammatory pain; Mol. Pain 4 31
5) Nonaka et al. (2017), A role for the locus coeruleus in the analgesic efficacy of N-acetylaspartylglutamate peptidase (GCPII) inhibitors ZJ43 and 2-PMPA; Mol.Pain 13 1
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