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Omega-conotoxin MVIIC

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ω-conotoxin MVIIC (omega conotoxin MVIIC) is a conotoxin that has been isolated from the venom of the cone Conus magus. ω-conotoxin MVIIC is a blocker of P/Q and N-type calcium channels.

Category

Peptide Inhibitors

Catalog number

BAT-015142

CAS number

147794-23-8

Molecular Formula

C106H178N40O32S7

Molecular Weight

2749.25

Specification
Reference Reading

IUPAC Name

2-[(1R,4S,7S,10S,13S,16S,19S,22R,27R,30S,36S,39S,45R,48S,54S,57R,62R,65S,71S,77S,83S)-62-amino-7,30,65,71-tetrakis(4-aminobutyl)-4,36,39-tris(3-carbamimidamidopropyl)-27-carbamoyl-10-[(1R)-1-hydroxyethyl]-48,54-bis(hydroxymethyl)-16-[(4-hydroxyphenyl)methyl]-77-methyl-13-(2-methylsulfanylethyl)-2,5,8,11,14,17,20,29,32,35,38,41,44,47,50,53,56,63,66,69,72,75,78,84,91-pentacosaoxo-24,25,59,60,87,88-hexathia-3,6,9,12,15,18,21,28,31,34,37,40,43,46,49,52,55,64,67,70,73,76,79,85,90-pentacosazatetracyclo[43.40.4.222,57.079,83]hennonacontan-19-yl]acetic acid

Synonyms

ω-Conotoxin MVIIC; L-cysteinyl-L-lysyl-glycyl-L-lysyl-glycyl-L-alanyl-L-prolyl-L-cysteinyl-L-arginyl-L-lysyl-L-threonyl-L-methionyl-L-tyrosyl-L-alpha-aspartyl-L-cysteinyl-L-cysteinyl-L-seryl-glycyl-L-seryl-L-cysteinyl-glycyl-L-arginyl-L-arginyl-glycyl-L-lysyl-L-cysteinamide (1->16),(8->20),(15->26)-tris(disulfide); H-Cys-Lys-Gly-Lys-Gly-Ala-Pro-Cys-Arg-Lys-Thr-Met-Tyr-Asp-Cys-Cys-Ser-Gly-Ser-Cys-Gly-Arg-Arg-Gly-Lys-Cys-NH2 (Disulfide bridge: Cys1-Cys16, Cys8-Cys20, Cys15-Cys26); SNX-230

Appearance

White lyophilized solid

Purity

≥97% by HPLC

Density

1.6±0.1 g/cm3

Sequence

CKGKGAPCRKTMYDCCSGSCGRRGKC-NH2 (Disulfide bridge: Cys1-Cys16, Cys8-Cys20, Cys15-Cys26)

Storage

Store at -20°C

Solubility

Soluble in Water, Saline

InChI

InChI=1S/C106H178N40O32S7/c1-53-103(178)146-36-15-23-75(146)101(176)144-74-52-185-183-49-71-89(164)126-43-79(154)130-62(21-13-34-120-105(115)116)90(165)133-60(20-12-33-119-104(113)114)87(162)124-42-78(153)129-61(18-6-10-31-109)91(166)140-70(83(112)158)48-181-184-51-73(100(175)143-72(99(174)139-68(45-147)88(163)125-44-80(155)131-69(46-148)97(172)141-71)50-182-180-47-57(111)84(159)132-59(17-5-9-30-108)86(161)123-41-77(152)128-58(16-4-8-29-107)85(160)122-40-76(151)127-53)142-96(171)67(39-81(156)157)138-95(170)66(38-55-24-26-56(150)27-25-55)137-93(168)65(28-37-179-3)136-102(177)82(54(2)149)145-94(169)63(19-7-11-32-110)134-92(167)64(135-98(74)173)22-14-35-121-106(117)118/h24-27,53-54,57-75,82,147-150H,4-23,28-52,107-111H2,1-3H3,(H2,112,158)(H,122,160)(H,123,161)(H,124,162)(H,125,163)(H,126,164)(H,127,151)(H,128,152)(H,129,153)(H,130,154)(H,131,155)(H,132,159)(H,133,165)(H,134,167)(H,135,173)(H,136,177)(H,137,168)(H,138,170)(H,139,174)(H,140,166)(H,141,172)(H,142,171)(H,143,175)(H,144,176)(H,145,169)(H,156,157)(H4,113,114,119)(H4,115,116,120)(H4,117,118,121)/t53-,54+,57-,58-,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,71-,72-,73-,74-,75-,82-/m0/s1

InChI Key

FHVUTHWUIUXZBY-QLANQDRJSA-N

Canonical SMILES

CC1C(=O)N2CCCC2C(=O)NC3CSSCC4C(=O)NCC(=O)NC(C(=O)NC(C(=O)NCC(=O)NC(C(=O)NC(CSSCC(C(=O)NC(CSSCC(C(=O)NC(C(=O)NCC(=O)NC(C(=O)NCC(=O)N1)CCCCN)CCCCN)N)C(=O)NC(C(=O)NCC(=O)NC(C(=O)N4)CO)CO)NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC(=O)C(NC3=O)CCCNC(=N)N)CCCCN)C(C)O)CCSC)CC5=CC=C(C=C5)O)CC(=O)O)C(=O)N)CCCCN)CCCNC(=N)N)CCCNC(=N)N

1. Omega-conotoxin MVIIC attenuates neuronal apoptosis in vitro and improves significant recovery after spinal cord injury in vivo in rats

Karen M Oliveira, et al. Int J Clin Exp Pathol. 2014 Jun 15;7(7):3524-36. eCollection 2014.

Excessive accumulation of intracellular calcium is the most critical step after spinal cord injury (SCI). Reducing the calcium influx should result in a better recovery from SCI. Calcium channel blockers have been shown a great potential in reducing brain and spinal cord injury. In this study, we first tested the neuroprotective effect of MVIIC on slices of spinal cord subjected to ischemia evaluating cell death and caspase-3 activation. Thereafter, we evaluated the efficacy of MVIIC in ameliorating damage following SCI in rats, for the first time in vivo. The spinal cord slices subjected a pretreatment with MVIIC showed a cell protection with a reduction of dead cells in 24.34% and of caspase-3-specific protease activation. In the in vivo experiment, Wistar rats were subjected to extradural compression of the spinal cord at the T12 vertebral level using a weigh of 70 g/cm, following intralesional treatment with either placebo or MVIIC in different doses (15, 30 and 60 pmol) five minutes after injury. Behavioral testing of hindlimb function was done using the Basso Beattie Bresnahan locomotor rating scale, and revealed significant recovery with 15 pmol (G15) compared to other trauma groups. Also, histological bladder structural revealed significant outcome in G15, with no morphological alterations, and anti-NeuN and TUNEL staining showed that G15 provided neuron preservation and indicated that this group had fewer neuron cell death, similar to sham. These results showed the neuroprotective effects of MVIIC in in vitro and in vivo model of SCI with neuronal integrity, bladder and behavioral improvements.

2. Combinatorial synthesis of omega-conotoxin MVIIC analogues and their binding with N- and P/Q-type calcium channels

T Sasaki, K Kobayashi, T Kohno, K Sato FEBS Lett. 2000 Jan 21;466(1):125-9. doi: 10.1016/s0014-5793(99)01772-x.

Omega-conotoxin MVIIC (MVIIC) blocks P/Q-type calcium channels with high affinity and N-type calcium channels with low affinity, while the highly homologous omega-conotoxin MVIIA blocks only N-type calcium channels. We wished to obtain MVIIC analogues more selective for P/Q-type calcium channels than MVIIC to elucidate structural differences among the channels, which discriminate the omega-conotoxins. To prepare a number of MVIIC analogues efficiently, we developed a combinatorial method which includes a random air oxidation step. Forty-seven analogues were prepared in six runs and some of them exhibited higher selectivity for P/Q-type calcium channels than MVIIC in binding assays.

3. Characteristics of omega-conotoxin GVI A and MVIIC binding to Cav 2.1 and Cav 2.2 channels captured by anti-Ca2+ channel peptide antibodies

Seiji Ichida, Junichi Abe, Kuniyo Komoike, Takashi Imanishi, Tetsuyuki Wada, Takashi Masuko, Takeshi Minami Neurochem Res. 2005 Apr;30(4):457-66. doi: 10.1007/s11064-005-2681-5.

A New Binding Method (NBM) was used to investigate the characteristics of the specific binding of 125I-omega-conotoxin (omega-CTX) GVIA and 125I-omega-CTX MVIIC to Cav2.1 and Cav2.2 channels captured from chick brain membranes by antibodies against B1Nt (a peptide sequence in Car2.1 and Cav2.2 channels). The results for the NBM were as follows. (1) The ED50 values for specific binding of 125I-omega-CTX GVIA and 125I-omega-CTX MVIIC to Cav2.1 and Cav2.2 channels were about 68 and 60 pM, respectively, and very similar to those (87 and 35 pM, respectively) to crude membranes from chick brain. (2) The specific 125I-omega-CTX GVIA (100 pM) binding was inhibited by omega-CTX GVIA (0.5 nM), dynorphine A (Dyn), gentamicin (Gen), neomycin (Neo) and tobramicin (Tob) (100 microM each), but not by omega-agaconotoxin (Aga) IVA, calciseptine, omega-CTX SVIB, omega-CTX MVIIC (0.5 nM each), PN200-110 (PN), diltiazem (Dil) or verapamil (Ver) (100 microM each). Calmodulin (CaM) inhibited the specific binding in a dose-dependent manner (IC50 value of about 100 microg protein/ml). (3) The specific 125I-omega-CTX MVIIC (60 pM) binding was inhibited by omega-CTX MVIIC, omega-CTX GVIA, omega-CTX SVIB (0.5 nM each), Dyn, Neo and Tob (100 microM, each), but not by omega-Aga IVA, calciseptine (0.5 nM each), PN, Dil, Ver (100 microM each) or 100 microg protein/ml CaM. These results suggested that the characteristics of the specific binding of 125I-omega-CTX GVIA and 125I-omega-CTX MVIIC to Cav2.1 and Cav2.2 channels in the NBM were very similar to those to crude membranes from chick brain, although the IC50 values for CaM and free Ca2+ of CaM were about 33- and 5000-fold higher, respectively, than those for the specific binding of 125I-omega-CTX GVIA and 125I-omega-CTX MVIIC to crude membranes.