MSG 606
目录号 : GC50303
MSG-606 对人黑皮质素 1 受体 (hMC1R) 具有强效拮抗活性和受体选择性（IC50 = 17 nM）。
Cas No.:1416983-77-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Animal experiment [1]: | |
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Animal models |
Male Sprague-Dawley (SD) rats |
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Preparation Method |
Rats were randomly divided into five groups: sham, SAH + vehicle 1(10 µl sterile saline, i.n), SAH + BMS-470539 (160 µg/kg, 10 µl), SAH + BMS-470539 + vehicle 2 (6 µl sterile saline, i.c.v), and SAH + BMS-470539 + MSG-606 (1 nmol/µl, 6 µl). MSG-606 was administered 1 h before SAH via i.c.v. route. Neurological testing was performed at 24 h after SAH. Ipsilateral/left cerebral cortex was sampled for western blotting. |
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Dosage form |
1 nmol/µl, 6 µl, i.c.v |
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Applications |
The inhibition of MC1R with MSG-606 significantly abolished the anti-inflammatory effects of BMS-470539 when compared to SAH + BMS-470539 + vehicle 2 group |
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References: [1]: Xu, W., Mo, J., Ocak, U. et al. Activation of Melanocortin 1 Receptor Attenuates Early Brain Injury in a Rat Model of Subarachnoid Hemorrhage viathe Suppression of Neuroinflammation through AMPK/TBK1/NF-κB Pathway in Rats. Neurotherapeutics 17, 294-308 (2020). https://doi.org/10.1007/s13311-019-00772-x | |
MSG-606 has potent antagonist activity and receptor selectivity for the human melanocortin 1 receptor (hMC1R) (IC50 = 17 nM) [1].
MSG-606 is an excellent probe for targeting specifically melanoma cells for skin cancer diagnosis. MSG-606 act as antagonist toward the melanoma cells. Binding and cAMP Activities of MSG-606 against Human Melanoma Cells (A375) with IC50 of 96 nM [1].
MSG-606 (1 nmol/μl, 6 μl) abolished the neuroprotective effects of the BMS-470539/MC1R system, in a subarachnoid hemorrhage (SAH) model [2].
References:
[1]:Cai M, Stankova M, Muthu D, et al. An unusual conformation of γ-melanocyte-stimulating hormone analogues leads to a selective human melanocortin 1 receptor antagonist for targeting melanoma cells[J]. Biochemistry, 2013, 52(4): 752-764.
[2]:Xu, W., Mo, J., Ocak, U. et al. Activation of Melanocortin 1 Receptor Attenuates Early Brain Injury in a Rat Model of Subarachnoid Hemorrhage viathe Suppression of Neuroinflammation through AMPK/TBK1/NF-κB Pathway in Rats. Neurotherapeutics 17, 294-308 (2020). https://doi.org/10.1007/s13311-019-00772-x
MSG-606 对人黑皮质素 1 受体 (hMC1R) 具有强效拮抗活性和受体选择性（IC50 = 17 nM）[1]。
MSG-606 是一种出色的探针,可专门针对黑色素瘤细胞进行皮肤癌诊断。 MSG-606 作为黑色素瘤细胞的拮抗剂。 MSG-606 对人黑色素瘤细胞 (A375) 的结合和 cAMP 活性,IC50 为 96 nM [1]。
MSG-606（1 nmol/μl,6 μl）在蛛网膜下腔出血 (SAH) 模型中消除了 BMS-470539/MC1R 系统的神经保护作用[2]。
| Cas No. | 1416983-77-1 | SDF | |
| Canonical SMILES | NC(=O)CNC(=O)[C@H](CC1=CC=CC=C1)NC(=O)[C@H](CCCNC(N)=N)NC(=O)[C@H](CC(O)=O)NC(=O)[C@@H]1CSCCCC(=O)NCC(=O)N[C@@H](CC2=CNC=N2)C(=O)N[C@@H](CC2=CC=CC=C2)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](CC2=CNC3=C2C=CC=C3)C(=O)N1 | ||
| 分子式 | C62H82N20O13S | 分子量 | 1347.51 |
| 溶解度 | Soluble in DMSO | 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 | 0.7421 mL | 3.7105 mL | 7.4211 mL |
| 5 mM | 0.1484 mL | 0.7421 mL | 1.4842 mL |
| 10 mM | 0.0742 mL | 0.3711 mL | 0.7421 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。
Melanocortin 1 receptor attenuates early brain injury following subarachnoid hemorrhage by controlling mitochondrial metabolism via AMPK/SIRT1/PGC-1αpathway in rats
Theranostics2021 Jan 1;11(2):522-539.PMID: 33391490DOI: 10.7150/thno.49426
Mitochondria-mediated oxidative stress and apoptosis contribute greatly to early brain injury (EBI) following subarachnoid hemorrhage (SAH). This study hypothesized that activation of melanocortin 1 receptor (MC1R), using BMS-470539, attenuates EBI by controlling mitochondrial metabolism after SAH. Methods: We utilized BMS-470539, MSG 606, selisistat, and PGC-1α to verify the neuroprotective effects of MC1R. We evaluated short- and long-term neurobehavior after SAH. Western blotting, immunofluorescence, and Golgi staining techniques were performed to assess changes in protein levels. Results: The results of western blotting suggested that the expression of SIRT1 and PGC-1α were increased, reaching their peaks at 24 h following SAH. Moreover, BMS-470539 treatment notably attenuated neurological deficits, and also reduced long-term spatial learning and memory impairments caused by SAH. The underlying neuroprotective mechanisms of the BMS-470539/MC1R system were mediated through the suppression of oxidative stress, apoptosis, and mitochondrial fission by increasing the levels of SIRT1, PGC-1α, UCP2, SOD, GPx, Bcl-2, cyto-Drp1, and ATP, while decreasing the levels of cleaved caspase-3, Bax, mito-Drp1, ROS, GSH/GSSG, and NADPH/NADP+ ratios. The neuroprotective effects of the BMS-470539/MC1R system were significantly abolished by MSG 606, selisistat, and PGC-1α siRNA. Conclusions: The activation of MC1R with BMS-470539 significantly attenuated EBI after SAH by suppressing the oxidative stress, apoptosis, and mitochondrial fission through the AMPK/SIRT1/PGC-1α signaling pathway.
Activation of Melanocortin 1 Receptor Attenuates Early Brain Injury in a Rat Model of Subarachnoid Hemorrhage viathe Suppression of Neuroinflammation through AMPK/TBK1/NF-κB Pathway in Rats
Neurotherapeutics2020 Jan;17(1):294-308.PMID: 31486022DOI: 10.1007/s13311-019-00772-x
Neuroinflammation plays a vital role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). The hypothesis of this study was that activation of melanocortin 1 receptor (MC1R) with BMS-470539 attenuates EBI by suppression of neuroinflammation after SAH. We utilized BMS-470539, MSG 606, and MRT-68601 to verify the neuroprotective effects of MC1R. We evaluated brain water content, short-term and long-term neurobehavior after SAH. Western blotting and immunofluorescence staining were utilized to assess the changes of protein levels. The results of western blotting suggested that the expressions of MC1R, phosphorylated-adenosine monophosphate-activated protein kinase (p-AMPK), and phosphorylated-TANK binding kinase 1 (p-TBK1) were increased and reached their peak points at 24 h following SAH. Moreover, BMS-470539 treatment notably attenuated neurological deficits caused by SAH, and also notably improved long-term spatial learning and memory abilities after SAH. The underlying mechanisms of the neuroprotection of BMS-470539 involved the suppression of microglia activation, promotion of CD206+ microglia transformation and reduction of neutrophil infiltration by increasing the levels of p-AMPK and p-TBK1 while decreasing the levels of NF-κB, IL-1β, and TNFα. The neuroprotective effects of BMS-470539 were significantly abolished by MSG 606 and MRT-68601. The activation of MC1R with BMS-470539 notably attenuates EBI after SAH by suppression of microglial activation and neutrophil infiltration via the AMPK/TBK1/NF-κB signaling pathway.