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M6690

Sigma-Aldrich

MDL 28170

≥90% (TLC)

Synonyme(s) :

Calpain Inhibitor III

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About This Item

Formule empirique (notation de Hill):
C22H26N2O4
Numéro CAS:
88191-84-8
Poids moléculaire :
382.45
Numéro MDL:
MFCD00798796
Code UNSPSC :
12352200
ID de substance PubChem :
24278565
Nomenclature NACRES :
NA.77

Pureté

≥90% (TLC)

Composition

Peptide Content, >90%

Solubilité

DMSO: 26 mg/mL
H2O: insoluble
methanol: soluble

Conditions d'expédition

wet ice

Température de stockage

2-8°C

Chaîne SMILES 

[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

Clé InChI

NGBKFLTYGSREKK-ANYOKISRSA-N

Informations sur le gène

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

Actions biochimiques/physiologiques

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.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, type N95 (US)

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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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
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
Amy L Clark et al.
Scientific reports, 7(1), 5611-5611 (2017-07-19)
Pro-inflammatory cytokines are important mediators of islet inflammation, leading to beta cell death in type 1 diabetes. Although alterations in both endoplasmic reticulum (ER) and cytosolic free calcium levels are known to play a role in cytokine-mediated beta cell death
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