M6690
MDL 28170
≥90% (TLC), calpain I and II inhibitor
Synonym(s):
Calpain Inhibitor III
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About This Item
Empirical Formula (Hill Notation):
C22H26N2O4
CAS Number:
Molecular Weight:
382.45
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Assay:
≥90% (TLC)
Quality level:
Product Name
MDL 28170, ≥90% (TLC)
Quality Level
assay
≥90% (TLC)
composition
Peptide Content, >90%
solubility
DMSO: 26 mg/mL, H2O: insoluble, methanol: soluble
shipped in
wet ice
storage temp.
2-8°C
SMILES string
[H]C(=O)C(Cc1ccccc1)NC(=O)[C@@H](NC(=O)OCc2ccccc2)C(C)C
InChI
1S/C22H26N2O4/c1-16(2)20(24-22(27)28-15-18-11-7-4-8-12-18)21(26)23-19(14-25)13-17-9-5-3-6-10-17/h3-12,14,16,19-20H,13,15H2,1-2H3,(H,23,26)(H,24,27)/t19?,20-/m0/s1
InChI key
NGBKFLTYGSREKK-ANYOKISRSA-N
Gene Information
human ... CAPN1(823), CAPN2(824)
Application
MDL 28170 has been used as a calpain inhibitor:
- to study its effects on neuroinflammation and necroptosis in rat model of cardiac arrest
- to analyze its effects on the degradation of neuronal nitric oxide synthase (nNOS) in beef semimembranosus muscle
- to study its protective effects against traumatic brain injury and survival of bone marrow-derived mesenchymal stem cells (BMSCs) in rat brain
Biochem/physiol Actions
MDL 28170 exhibits neuroprotective effects against spinal cord injury, focal cerebral ischemia, and neonatal hypoxia-ischemia in rats. It also shows anti-inflammatory and anti-neurodegenerative properties. MDL 28170 crosses the blood-brain barrier and penetrates readily through the cell membranes.
MDL 28170 is a potent cell permeable calpain I and II inhibitor; reduces capsaicin-mediated cell death in cultured dorsal root ganglion neurons. Reduced occurrence of apoptosis in H2O2 and A23187 treated PC12 cells. γ-secretase-inhibitor.
Potent cell permeable calpain I and II inhibitor; reduces capsaicin-mediated cell death in cultured dorsal root ganglion neurons.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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Wen-Yan Wang et al.
International immunopharmacology, 93, 107377-107377 (2021-02-01)
Cerebral ischemia-reperfusion injury (CIRI) is the leading cause of poor neurological prognosis after cardiopulmonary resuscitation (CPR). We previously reported that the extracellular signal-regulated kinase (ERK) activation mediates CIRI. Here, we explored the potential ERK/calpain-2 pathway role in CIRI using a
Jiangnan Hu et al.
Stem cell research & therapy, 10(1), 96-96 (2019-03-17)
Studies have shown that transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) protects against brain damage. However, the low survival number of transplanted BMSCs remains a pertinent challenge and can be attributed to the unfavorable microenvironment of the injured brain.
Stephanie N Thompson et al.
Journal of neurotrauma, 27(12), 2233-2243 (2010-09-30)
The cytoskeletal and neuronal protective effects of early treatment with the blood-brain barrier- and cell-permeable calpain inhibitor MDL-28170 was examined in the controlled cortical impact (CCI) traumatic brain injury (TBI) model in male CF-1 mice. This was preceded by a