DPDPE (trifluoroacetate salt)
(Synonyms: D-Pen2,D-Pen5Enkephalin) 目录号 : GC43568
A synthetic pepetide δ-opioid receptor agonist
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
DPDPE is a synthetic enkephalin peptide and δ-opioid receptor agonist (Ki = 2.7 nM in rat brain homogenates). DPDPE has greater than 250-fold selectivity for the δ-opioid receptor over the μ- and κ-opioid receptors in rat brain homogenates (Kis = 713 and >1,500 nM, respectively). It also selectively inhibits electrically-evoked contractions in mouse vas deferens over guinea pig myenteric plexus (IC50s = 4.14 and 3,000 nM, respectively), which does not express the δ-opioid receptor. In vivo, DPDPE (140 nmol, i.v.) completely blocks tonic hindlimb extension induced by maximal electroshock (MES) in 50% of tested rats and increases the flurothyl-induced seizure threshold by 15-20% in rats, effects that can be blocked by the selective δ-opioid receptor antagonist ICI 154129. DPDPE (1-10 μg, i.v) dose-dependently reduces formalin-induced paw licking and lifting, indicating analgesia, in rats. However, DPDPE (15 μg, i.v.) increases the latency to tail withdrawal in the tail-immersion test in both wild-type and δ-opioid receptor knockout mice by 6.74 and 7.6 seconds, respectively, compared to a saline control, but not in μ-opioid receptor knockout mice, and the effect can be blocked by the μ-opioid receptor antagonist CTOP.
| Cas No. | SDF | ||
| 别名 | D-Pen2,D-Pen5Enkephalin | ||
| Canonical SMILES | CC([C@H](C(O)=O)NC1=O)(C)SSC(C)(C)[C@@H](NC([C@@H](N)CC2=CC=C(O)C=C2)=O)C(NCC(N[C@H]1CC3=CC=CC=C3)=O)=O.FC(F)(C(O)=O)F | ||
| 分子式 | C30H39N5O7S2•XCF3COOH | 分子量 | 645.8 |
| 溶解度 | Water: 1 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5485 mL | 7.7423 mL | 15.4847 mL |
| 5 mM | 0.3097 mL | 1.5485 mL | 3.0969 mL |
| 10 mM | 0.1548 mL | 0.7742 mL | 1.5485 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The role of nitric oxide in the local antiallodynic and antihyperalgesic effects and expression of delta-opioid and cannabinoid-2 receptors during neuropathic pain in mice
J Pharmacol Exp Ther 2010 Sep 1;334(3):887-96.PMID:20498253DOI:10.1124/jpet.110.167585
Both delta-opioid receptor (DOPr) and cannabinoid-2 receptor (CB2R) agonists attenuate neuropathic pain, but the precise mechanism implicated in these effects is not completely elucidated. We investigated whether nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric-oxide synthases could modulate DOPr and/or CB2R antiallodynic and antihyperalgesic effects through the peripheral nitric oxide-cGMP-protein kinase G (PKG) pathway activation and affect their expression during neuropathic pain. In wild-type (WT) mice at 21 days after chronic constriction of sciatic nerve, we evaluated the effects of [d-Pen(2),d-Pen(5)]-enkephalin (DPDPE); (2-methyl-1-propyl-1H-indol-3-yl)-1-naphthalenylmethanone (JWH-015); and a NOS1 [N-[(4S)-4-amino-5-[(2-aminoethyl)amino]pentyl]-N'-nitroguanidine tris(trifluoroacetate) salt; NANT], NOS2 [l-N(6)-(1-iminoethyl)-lysine; l-NIL], l-guanylate cyclase [1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; ODQ], or PKG [(Rp)-8-(para-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate; Rp-8-pCPT-cGMPs] inhibitor administered alone or combined. Expression of DOPr and CB2R mRNA in the spinal cord and dorsal root ganglia of naive and nerve-injured WT, NOS1-knockout (KO), and NOS2-KO mice, also was assessed. The subplantar administration of NANT, l-NIL, ODQ, or Rp-8-pCPT-cGMPs dose-dependently inhibited neuropathic pain and enhanced the local effects of DPDPE or JWH-015. Moreover, although the basal levels of DOPr and CB2R mRNA were similar between WT and NOS-KO animals, nerve injury only decreased (DOPr) or increased (CB2R) their expression in the dorsal root ganglia of WT and NOS2-KO mice, and not in NOS1-KO mice. Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.