MG-101 - CAS 110044-82-1
Catalog number: 110044-82-1
Category: Inhibitor
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Molecular Formula:
C20H37N3O4
Molecular Weight:
383.53
COA:
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Targets:
Proteasome
Description:
MG-101, also known as Calpain Inhibitor I and ALLN, is a calpain inhibitor (IC50 = 0.09 μM) that activates p53-dependent apoptosis in tumor cell lines. Activities of MG-101 includes: (1) reduce colon injury caused by dinitrobenzene sulphonic acid; (2) overcome acquired resistance to TRAIL; (3) protect against atractyloside-induced toxicity. (4). reduce colon injury caused by dinitrobenzene sulphonic acid.
Purity:
0.98
Appearance:
white solid powder
Synonyms:
Calpain Inhibitor I; MG-101; MG 101; MG101; ALLN; Ac-LLnL-CHO, N-Acetyl-Leu-Leu-Norleu-al, N-Acetyl-L-leucyl-L-leucyl-L-norleucinal. Beilstein Registry Number 7656053; MDL number MFCD00065505; PubChem Substance ID 24852739
MSDS:
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InChIKey:
FMYKJLXRRQTBOR-BZSNNMDCSA-N
InChI:
InChI=1S/C20H37N3O4/c1-7-8-9-16(12-24)22-19(26)18(11-14(4)5)23-20(27)17(10-13(2)3)21-15(6)25/h12-14,16-18H,7-11H2,1-6H3,(H,21,25)(H,22,26)(H,23,27)/t16-,17-,18-/m0/s1
Canonical SMILES:
CCCCC(C=O)NC(=O)C(CC(C)C)NC(=O)C(CC(C)C)NC(=O)C
1.Rhein triggers apoptosis via induction of endoplasmic reticulum stress, caspase-4 and intracellular calcium in primary human hepatic HL-7702 cells.
KoraMagazi A;Wang D;Yousef B;Guerram M;Yu F Biochem Biophys Res Commun. 2016 Apr 22;473(1):230-236. doi: 10.1016/j.bbrc.2016.03.084. Epub 2016 Mar 19.
Rhein is an active component of rhubarb; a traditional Chinese medicine reported to induce apoptosis and cause liver toxicity. However, rhein's apoptotic-inducing effects, as well as its molecular mechanisms of action on hepatic cells need to be further explored. In the present study, rhein was found to trigger apoptosis in primary human hepatic HL-7702 cells as showed by annexin V/PI double staining assay and nuclear morphological changes demonstrated by Hoechst 33258 staining. Moreover, it was observed that the mechanism implicated in rhein-induced apoptosis was caspase-dependent, presumably via ER-stress associated pathways, as illustrated by up-regulation of glucose-regulated protein 78 (GRP 78), PKR-like ER kinase (PERK), C-Jun N-terminal kinase (JNK) and CCAAT/enhancer-binding protein homologous protein (CHOP). Meanwhile, caspase-4 as a hallmark of ER-stress, was also showed to be activated following by caspase-3 activation. Furthermore, rhein also promoted intracellular elevation of calcium that contributed in apoptosis induction. Interestingly, pre-treatment with calpain inhibitor I reduced the effects of rhein on apoptosis induction and JNK activation. These data suggested that rhein-induced apoptosis through ER-stress and elevated intracellular calcium level in HL-7702 cells.
2.Rapid increase in immunoreactivity to GFAP in astrocytes in vitro induced by acidic pH is mediated by calcium influx and calpain I.
Lee YB;Du S;Rhim H;Lee EB;Markelonis GJ;Oh TH Brain Res. 2000 May 12;864(2):220-9.
In higher vertebrates, reactive gliosis resulting from injury to the central nervous system (CNS) is characterized by a rapid increase in immunoreactivity (IR) to glial fibrillary acidic protein (GFAP). Little is known about the extracellular signals that initiate the increase in GFAP-IR following CNS injury. We demonstrated recently [T.H. Oh, G.J. Markelonis, J.R. Von Visger, B. Baik, M.T. Shipley, Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes, Glia 13 (1995) 319-322] that a rapid increase in GFAP-IR can be evoked in mature astrocyte cultures by exposing the cells to an acidic medium. We investigated the intracellular pathway(s) involved in initiating increased GFAP-IR, a hallmark of reactive astrocytes. The increase in GFAP-IR produced by exposure to acidic medium was blocked by pretreatment with nickel ions, by such blockers of L-type calcium channels as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium chelator, BAPTA-AM. At physiological pH, treatment with the calcium ionophore, A23187, resulted in increased GFAP-IR which could be blocked by pretreatment with calpain inhibitor I.
3.Phenotypical characteristics, biochemical pathways, molecular targets and putative role of nitric oxide-mediated programmed cell death in Leishmania.
Holzmuller P;Bras-Gonçalves R;Lemesre JL Parasitology. 2006;132 Suppl:S19-32.
Nitric oxide (NO) has been demonstrated to be the principal effector molecule mediating intracellular killing of Leishmania, both in vitro and in vivo. We investigated the type of cell death process induced by NO for the intracellular amastigote stage of the protozoa Leishmania. Specific detection methods revealed a rapid and extensive cell death with morphological features of apoptosis in axenic amastigotes exposed to NO donors, in intracellular amastigotes inside in vitro - activated mouse macrophages and also in activated macrophages of regressive lesions in a leishmaniasis-resistant mouse model. We extended our investigations to the dog, a natural host-reservoir of Leishmania parasites, by demonstrating that co-incubation of infected macrophages with autologous lymphocytes derived from dogs immunised with purified excreted-secreted antigens of Leishmania resulted in a significant NO-mediated apoptotic cell death of intracellular amastigotes. From the biochemical point of view, NO-mediated Leishmania amastigotes apoptosis did not seem to be controlled by caspase activity as indicated by the lack of effect of cell permeable inhibitors of caspases and cysteine proteases, in contrast to specific proteasome inhibitors, such as lactacystin or calpain inhibitor I.
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CAS 110044-82-1 MG-101

MG-101
(CAS: 110044-82-1)

MG-101, also known as Calpain Inhibitor I and ALLN, is a calpain inhibitor (IC50 = 0.09 μM) that activates p53-dependent apoptosis in tumor cell lines. Activiti...

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CAS 110044-82-1 MG-101

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