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78123-71-4

中文名稱 L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺
英文名稱 DAGO
CAS 78123-71-4
分子式 C26H35N5O6
分子量 513.59
MOL 文件 78123-71-4.mol
更新日期 2026/07/22 14:17:39
78123-71-4 結(jié)構(gòu)式 78123-71-4 結(jié)構(gòu)式

基本信息

中文別名
化合物DAMGO
L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺
英文別名
DAGO
DAMGO
Dagol
Damge
DAMPGO
RX-783006
NIH 10891
M.W. 513.59 C26H35N5O6
Tyr-D-Ala-Gly-MePhe-Gly-ol
H-Tyr-D-Ala(Me)Phe-NH-CH2-OH
所屬類別
生物化工:激動(dòng)劑抑制劑

物理化學(xué)性質(zhì)

沸點(diǎn)922.7±65.0 °C(Predicted)
密度1.271±0.06 g/cm3(Predicted)
儲(chǔ)存條件-15°C
溶解度≥40.7 mg/mL in EtOH; ≥40.7 mg/mL in H2O; ≥42.2 mg/mL in DMSO
酸度系數(shù)(pKa)9.97±0.15(Predicted)
形態(tài)固體
顏色白色
水溶解性Soluble in water (4 mM)
序列H-Tyr-D-Ala-Gly-NMe-Phe-Gly-ol
穩(wěn)定性吸濕性
InChIKeyHPZJMUBDEAMBFI-RZPISPKSNA-N
SMILES[C@H](C(=O)NCCO)(N(C)C(=O)CNC(=O)[C@@H](C)NC(=O)[C@@H](N)CC1C=CC(O)=CC=1)CC1C=CC=CC=1 |&1:0,15,20,r|

應(yīng)用領(lǐng)域

參考質(zhì)量標(biāo)準(zhǔn)
外觀:白色粉末
純度(HPLC) ≥98.0%
醋酸根含量≤12.0%
水分含量≤8.0%
肽含量≥80.0%
內(nèi)毒素≤50EU/mg
氨基酸組成分析≤±10%
L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱CAS號(hào)包裝價(jià)格
2026/06/05HY-P0210L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺
DAMGO
78123-71-41mg600元
2026/06/05HY-P0210L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺
DAMGO
78123-71-45mg990元
2026/06/05HY-P0210L-酪氨酰-D-丙氨酰甘氨酰-N-(2-羥基乙基)-NALPHA-甲基-L-苯丙氨酰胺
DAMGO
78123-71-410mg1700元

常見(jiàn)問(wèn)題列表

生物活性
DAMGO 是 一種選擇性的 μ-阿片受體 (μ-OPR) 激動(dòng)劑,Kd 值為 3.46 nM。
靶點(diǎn)

Kd: 3.46±0.84 nM (native μ-OPR)

體外研究

DAMGO, a μ-opioid receptor selective agonist, distinguishes between μ- and δ-opioid receptors around their first extracellular loops. In native μ-OPR, the K d value for DAMGO is 3.46± 0.84 nM (n=3). The chimeric receptor MMDD, in which the carboxy-terminal half of μ-OPR is replaced with the corresponding region of δ-OPR, exhibits an equivalent affinity (K d =2.13±0.40 nM; n=3) to DAMGO compared with the native μ-OPR. DAMGO is a selective μ-opioid peptide. DAMGO abolishes the neuroprotective effect of CXCL12 in N-methyl-d-aspartate (NMDA) neurotoxicity studies. Regulation of neuronal response to CXCL12 is essential for shaping of developing and mature central nervous system (CNS). To establish whether DAMGO alter the effect of CXCL12 on neuronal survival, the ability of CXCL12 to protect neurons from N-methyl-d-aspartate (NMDA)-induced death is examined in the presence and absence of DAMGO. Cortical cultures are treated with DAMGO (1 and 10 μM). Neurons are subsequently exposed to NMDA (20 min) and/or CXCL12 (added 10 min before NMDA) in the absence of glia and then returned to the original culture dishes with the glial feeder layer. Neuronal death is evaluated after 24 h. DAMGO inhibits neuronal survival promoted by CXCL12.

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