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MOG (35-55)

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(MOG) 35-55 is a minor component of CNS myelin. Produces a relapsing-remitting neurological disease with extensive plaque-like demyelination.

Category

Peptide Inhibitors

Catalog number

BAT-010068

CAS number

149635-73-4

Molecular Formula

C118H177N35O29S

Molecular Weight

2581.95

Size	Price	Stock	Quantity
5 mg	$259	In stock

Specification
Reference Reading

IUPAC Name

(2S)-6-amino-2-[[2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-4-methylsulfanylbutanoyl]amino]-4-carboxybutanoyl]amino]-3-methylbutanoyl]amino]acetyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-hydroxypropanoyl]pyrrolidine-2-carbonyl]amino]-3-phenylpropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-methylbutanoyl]amino]-3-methylbutanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-oxobutanoyl]amino]acetyl]amino]hexanoic acid

Synonyms

MOG35-55

Purity

>98%

Density

1.48±0.1 g/cm3(Predicted)

Sequence

MEVGWYRSPFSRVVHLYRNGK

Storage

Store at -20°C

InChI

InChI=1S/C118H177N35O29S/c1-61(2)47-80(103(169)143-81(49-66-30-34-70(156)35-31-66)104(170)139-75(26-17-42-129-116(122)123)99(165)145-86(53-90(121)158)98(164)133-56-91(159)136-79(115(181)182)25-15-16-41-119)142-108(174)85(52-69-55-128-60-135-69)147-112(178)95(63(5)6)152-113(179)96(64(7)8)151-101(167)77(28-19-44-131-118(126)127)141-109(175)87(58-154)148-106(172)83(48-65-21-11-10-12-22-65)146-110(176)89-29-20-45-153(89)114(180)88(59-155)149-100(166)76(27-18-43-130-117(124)125)140-105(171)82(50-67-32-36-71(157)37-33-67)144-107(173)84(51-68-54-132-74-24-14-13-23-72(68)74)137-92(160)57-134-111(177)94(62(3)4)150-102(168)78(38-39-93(161)162)138-97(163)73(120)40-46-183-9/h10-14,21-24,30-37,54-55,60-64,73,75-89,94-96,132,154-157H,15-20,25-29,38-53,56-59,119-120H2,1-9H3,(H2,121,158)(H,128,135)(H,133,164)(H,134,177)(H,136,159)(H,137,160)(H,138,163)(H,139,170)(H,140,171)(H,141,175)(H,142,174)(H,143,169)(H,144,173)(H,145,165)(H,146,176)(H,147,178)(H,148,172)(H,149,166)(H,150,168)(H,151,167)(H,152,179)(H,161,162)(H,181,182)(H4,122,123,129)(H4,124,125,130)(H4,126,127,131)/t73-,75-,76-,77-,78-,79-,80-,81-,82-,83-,84-,85-,86-,87-,88-,89-,94-,95-,96-/m0/s1

InChI Key

JMTCEFUSRHYJBF-DDJPMISGSA-N

Canonical SMILES

CC(C)CC(C(=O)NC(CC1=CC=C(C=C1)O)C(=O)NC(CCCNC(=N)N)C(=O)NC(CC(=O)N)C(=O)NCC(=O)NC(CCCCN)C(=O)O)NC(=O)C(CC2=CNC=N2)NC(=O)C(C(C)C)NC(=O)C(C(C)C)NC(=O)C(CCCNC(=N)N)NC(=O)C(CO)NC(=O)C(CC3=CC=CC=C3)NC(=O)C4CCCN4C(=O)C(CO)NC(=O)C(CCCNC(=N)N)NC(=O)C(CC5=CC=C(C=C5)O)NC(=O)C(CC6=CNC7=CC=CC=C76)NC(=O)CNC(=O)C(C(C)C)NC(=O)C(CCC(=O)O)NC(=O)C(CCSC)N

1.Role of orexin-A in experimental autoimmune encephalomyelitis.

Fatemi I1, Shamsizadeh A1, Ayoobi F1, Taghipour Z1, Sanati MH2, Roohbakhsh A3, Motevalian M4. J Neuroimmunol. 2016 Feb 15;291:101-9. doi: 10.1016/j.jneuroim.2016.01.001. Epub 2016 Jan 8.

The aim of this study was to evaluate the effects of orexin-A (OX-A) on behavioral and pathological parameters and on gene expression of some multiple sclerosis-related peptides in a model of experimental autoimmune encephalomyelitis (EAE). EAE was induced by subcutaneous administration of MOG 35-55. Following immunization, the treatment was initiated by using SB.334867 (orexin-1 receptor antagonist) and/or OX-A. Locomotor activity and exploratory behaviors were monitored using open field and T-maze continuous alternation task (T-CAT) respectively. Pain sensitivity was assessed by hot-plate test. Histopathological assessments were performed by H&E staining. The expression of TGF-β, MBP, MMP-9, IL-12, iNOS and MCP-1 were measured using real-time PCR method in lumbar spinal cord. OX-A administration in EAE mice remarkably attenuated the clinical symptoms, increased latency response in hot plate test, inhibited infiltration of inflammatory cells, up-regulated mRNA expression of TGF-β as well as MBP and down-regulated mRNA expression of iNOS, MMP-9 and IL-12.

2.RGS10 deficiency ameliorates the severity of disease in experimental autoimmune encephalomyelitis.

Lee JK1, Kannarkat GT2, Chung J3, Joon Lee H2, Graham KL2, Tansey MG2. J Neuroinflammation. 2016 Feb 1;13(1):24. doi: 10.1186/s12974-016-0491-0.

BACKGROUND: Regulator of G-protein signaling (RGS) family proteins, which are GTPase accelerating proteins (GAPs) that negatively regulate G-protein-coupled receptors (GPCRs), are known to be important modulators of immune cell activation and function. Various single-nucleotide polymorphisms in RGS proteins highly correlate with increased risk for multiple sclerosis (MS), an autoimmune, neurodegenerative disorder. An in-depth search of the gene expression omnibus profile database revealed higher levels of RGS10 and RGS1 transcripts in peripheral blood mononuclear cells (PBMCs) in MS patients, suggesting potential functional roles for RGS proteins in MS etiology and/or progression.

3.CNS accumulation of regulatory B cells is VLA-4-dependent.

Lehmann-Horn K1, Sagan SA1, Winger RC1, Spencer CM1, Bernard CC1, Sobel RA1, Zamvil SS1. Neurol Neuroimmunol Neuroinflamm. 2016 Mar 9;3(2):e212. doi: 10.1212/NXI.0000000000000212. eCollection 2016.

OBJECTIVE: To investigate the role of very late antigen-4 (VLA-4) on regulatory B cells (Breg) in CNS autoimmune disease.

4.Effect of Bushen Yisui Capsule () on oligodendrocyte lineage genes 1 and 2 in mice with experimental autoimmune encephalomyelitis.

Yang T1, Zheng Q2,3, Zhao H2, Zhang QX2, Li M2, Qi F2, Li KN1, Fang L2, Wang L4, Fan YP5. Chin J Integr Med. 2016 Feb 26. [Epub ahead of print]

OBJECTIVE: To study the effects of Bushen Yisui Capsule (, BSYSC) on the oligodendrocyte lineage genes (Olig) 1 and Olig2 in C57BL/6 mice with experimental autoimmune encephalomyelitis (EAE) in order to explore the remyelination effect of BSYSC.