| CAS NO: | 88191-84-8 |
| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| Physical Appearance | A solid |
| Storage | Store at -20°C |
| M.Wt | 382.45 |
| Cas No. | 88191-84-8 |
| Formula | C22H26N2O4 |
| Solubility | insoluble in H2O; ≥16.75 mg/mL in DMSO; ≥25.05 mg/mL in EtOH with ultrasonic |
| Chemical Name | benzyl N-[(2S)-3-methyl-1-oxo-1-[(1-oxo-3-phenylpropan-2-yl)amino]butan-2-yl]carbamate |
| Canonical SMILES | CC(C)C(C(=O)NC(CC1=CC=CC=C1)C=O)NC(=O)OCC2=CC=CC=C2 |
| 运输条件 | 蓝冰运输或根据您的需求运输。 |
| 一般建议 | 为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。 |
MDL 28170是一种选择性的抑制剂，抑制calpain和cathepsin B，Ki值分别为10和25 nM，而不抑制胰蛋白酶样丝氨酸蛋白酶。MDL 28170可以快速通过血脑屏障，在全身给药后可抑制脑内半胱氨酸蛋白酶的活性[1，2]。
Calpain可通过直接限制肌节的蛋白水解，从而影响再灌注功能。再灌注期间，MDL-28170的功能改善得到实验的支持。MDL-28170通过阻断calpains的催化位点而起作用。实验也表明，皮肤肌纤维减少了对Ca2+的敏感性，而在缺血之前或再灌注的早期给予MDL-28170治疗可恢复敏感性[1]。
小鼠腹腔巨噬细胞用trypomastigotes预感染3小时，MDL28170能够显著减少血流中trypomastigotes的生存能力，IC50/24 h值为20.4 mM。在感染巨噬细胞之前，寄生虫用6.25-50 mM的MDL28170预处理呈现明显的剂量依赖性抑制，相应的抑制从20%增加到50%。此外，实验感染T. Cruzi的巨噬细胞用MDL 28170处理减少了感染的百分比，即使在6.25 mM的最低浓度时[3]。
在离体大鼠心脏中，一旦Ca2+饱食，心脏立即恶化，揭示了心脏功能的显著抑制和心肌损伤区域的扩大，并伴随乳酸脱氢酶、线粒体释放细胞色素c、凋亡指数及降解肌钙蛋白（TnI）的显著增加。MDL 28170显著抑制这些变化，除了肌钙蛋白的降解[4]。
参考文献：
1. Urthaler F, Wolkowicz PE, Digerness SB, et al. MDL-28170, a membrane-permeantcalpain inhibitor, attenuates stunning and PKC epsilon proteolysis in reperfused ferret hearts. Cardiovasc Res, 1997, 35 (1): 60-7.
2. Li P, Wendy H, He Q, et al. Postischemic treatment withcalpain inhibitor MDL 28170ameliorates brain damage in a gerbil model of global ischemia, Neuroscience Letters, 1998, 247 :17–20.
3. V?´tor EV, Rubem F, Andre´ L, Effects of the calpain inhibitor MDL28170 on the clinically relevant forms of Trypanosomacruzi in vitro. J AntimicrobChemother , 2010, 65: 1395–1398.
4. Bi S H, Jin Z X, Zhang J Y, et al. Calpaininhibi tor MDL 28170 protectsagainst the Ca2+paradox in rat hearts.Clinical and Experimental Pharmacology and Physiology , 2012, 39:385–392 .
| Cell experiment:[1] | |
Cell lines | Schwann cells |
Reaction Conditions | 50 nM, 500 nM, 5 μM, or 50 μM MDL 28170 for 4 h incubation |
Applications | MDL 28170 significantly enhanced Schwann cell survivalin vitroin response to oxidative stress induced by application of H2O2, without reducing lactate dehydrogenase release. |
| Animal experiment:[2] | |
Animal models | A gerbil model of global ischemia |
Dosage form | 50 mg/kg Injected at 0.5 and 3 h of recirculation following 5 min of global ischemia |
Applications | The calpain inhibitor, MDL 28170, protected against cortical neuronal damage even if the treatment was delayed until 3 h after reperfusion. However, the neuroprotective effect of this agent was less pronounced in the hippocampal CA1 sector. |
Note | The technical data provided above is for reference only. |
References: 1. Hill CE, Guller Y, Raffa SJ, et al. A calpain inhibitor enhances the survival of Schwann cells in vitro and after transplantation into the injured spinal cord. Journal of Neurotrauma, 2010, 27(9): 1685-1695. 2. Li PA, Howlett W, He QP, et al. Postischemic treatment with calpain inhibitor MDL 28170 ameliorates brain damage in a gerbil model of global ischemia. Neuroscience Letters, 1998, 247(1): 17-20. | |
| MDL 28170是一种有效的和选择性的calpain和cathepsin B抑制剂，Ki值分别为10和25 nM，而不抑制胰蛋白酶样丝氨酸蛋白酶。 | ||||||
| 靶点 | calpain | cathepsin B | ||||
| IC50 | 10nM | 25nM | ||||
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