MilliporeSigma
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M6690

Sigma-Aldrich

MDL 28170

≥90% (TLC)

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Synonym(s):
Calpain Inhibitor III
Empirical Formula (Hill Notation):
C22H26N2O4
CAS Number:
88191-84-8
Molecular Weight:
382.45
MDL number:
MFCD00798796
PubChem Substance ID:
24278565
NACRES:
NA.77

Quality Level

200

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)

Amino Acid Sequence

Z-Val-Phe-al

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.

Storage Class Code

13 - Non Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificate of Analysis

Enter Lot Number to search for Certificate of Analysis (COA).

Certificate of Origin

Enter Lot Number to search for Certificate of Origin (COO).

More Documents

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Quotes and Ordering

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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.
Lorelei B Silverman-Gavrila et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 33(5), 1975-1990 (2013-02-01)
Low-frequency depression (LFD) of transmitter release occurs at phasic synapses with stimulation at 0.2 Hz in both isolated crayfish (Procambarus clarkii) neuromuscular junction (NMJ) preparations and in intact animals. LFD is regulated by presynaptic activity of the Ca(2+)-dependent phosphatase calcineurin
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
Gernot Walko et al.
PLoS genetics, 7(12), e1002396-e1002396 (2011-12-07)
Autosomal recessive mutations in the cytolinker protein plectin account for the multisystem disorders epidermolysis bullosa simplex (EBS) associated with muscular dystrophy (EBS-MD), pyloric atresia (EBS-PA), and congenital myasthenia (EBS-CMS). In contrast, a dominant missense mutation leads to the disease EBS-Ogna
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
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