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IKKγ NBD Inhibitory Peptide

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IKKγ NBD Inhibitory Peptide is a NEMO-binding domain peptide (NBD peptide) corresponding to the NEMO amino-terminal alpha-helical region and has been shown to block TNF-α-induced NF-kB activation.

Category

Peptide Inhibitors

Catalog number

BAT-009255

CAS number

372146-18-4

Molecular Formula

C170H259N49O42S

Molecular Weight

3693.23

Specification
Reference Reading

IUPAC Name

(2S)-2-[[(2S,3R)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-6-amino-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-6-amino-2-[[(2S,3S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-carboxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoyl]amino]-3-methylpentanoyl]amino]hexanoyl]amino]-3-methylpentanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-phenylpropanoyl]amino]-5-oxopentanoyl]amino]-4-oxobutanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylsulfanylbutanoyl]amino]hexanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]hexanoyl]amino]hexanoyl]amino]-3-hydroxybutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-hydroxybutanoyl]amino]pentanedioic acid

Synonyms

Asp-Arg-Gln-Ile-Lys-Ile-Trp-Phe-Gln-Asn-Arg-Arg-Met-Lys-Trp-Lys-Lys-Thr-Ala-Leu-Asp-Trp-Ser-Trp-Leu-Gln-Thr-Glu; L-alpha-aspartyl-L-arginyl-L-glutaminyl-L-isoleucyl-L-lysyl-L-isoleucyl-L-tryptophyl-L-phenylalanyl-L-glutaminyl-L-asparagyl-L-arginyl-L-arginyl-L-methionyl-L-lysyl-L-tryptophyl-L-lysyl-L-lysyl-L-threonyl-L-alanyl-L-leucyl-L-alpha-aspartyl-L-tryptophyl-L-seryl-L-tryptophyl-L-leucyl-L-glutaminyl-L-threonyl-L-glutamic acid

Purity

>98%

Sequence

DRQIKIWFQNRRMKWKKTALDWSWLQTE

Storage

Store at -20°C

Solubility

Soluble in Water

InChI

InChI=1S/C170H259N49O42S/c1-13-88(7)136(217-151(244)115(55-59-130(177)224)200-143(236)111(51-34-67-186-168(180)181)194-141(234)102(175)78-134(229)230)163(256)204-110(50-29-33-66-174)149(242)216-137(89(8)14-2)164(257)214-125(77-97-84-192-106-46-25-21-42-101(97)106)158(251)208-121(73-93-37-16-15-17-38-93)155(248)201-114(54-58-129(176)223)147(240)212-126(79-132(179)226)160(253)199-113(53-36-69-188-170(184)185)144(237)197-112(52-35-68-187-169(182)183)145(238)203-117(62-70-262-12)148(241)195-108(48-27-31-64-172)146(239)209-122(74-94-81-189-103-43-22-18-39-98(94)103)156(249)198-107(47-26-30-63-171)142(235)196-109(49-28-32-65-173)150(243)218-138(91(10)221)165(258)193-90(9)140(233)206-119(71-86(3)4)154(247)213-127(80-135(231)232)161(254)210-124(76-96-83-191-105-45-24-20-41-100(96)105)159(252)215-128(85-220)162(255)211-123(75-95-82-190-104-44-23-19-40-99(95)104)157(250)207-120(72-87(5)6)153(246)202-116(56-60-131(178)225)152(245)219-139(92(11)222)166(259)205-118(167(260)261)57-61-133(227)228/h15-25,37-46,81-84,86-92,102,107-128,136-139,189-192,220-222H,13-14,26-36,47-80,85,171-175H2,1-12H3,(H2,176,223)(H2,177,224)(H2,178,225)(H2,179,226)(H,193,258)(H,194,234)(H,195,241)(H,196,235)(H,197,237)(H,198,249)(H,199,253)(H,200,236)(H,201,248)(H,202,246)(H,203,238)(H,204,256)(H,205,259)(H,206,233)(H,207,250)(H,208,251)(H,209,239)(H,210,254)(H,211,255)(H,212,240)(H,213,247)(H,214,257)(H,215,252)(H,216,242)(H,217,244)(H,218,243)(H,219,245)(H,227,228)(H,229,230)(H,231,232)(H,260,261)(H4,180,181,186)(H4,182,183,187)(H4,184,185,188)/t88-,89-,90-,91+,92+,102-,107-,108-,109-,110-,111-,112-,113-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,136-,137-,138-,139-/m0/s1

InChI Key

MJLJQYXWQIGWNE-FHKTVDBHSA-N

Canonical SMILES

CCC(C)C(C(=O)NC(CCCCN)C(=O)NC(C(C)CC)C(=O)NC(CC1=CNC2=CC=CC=C21)C(=O)NC(CC3=CC=CC=C3)C(=O)NC(CCC(=O)N)C(=O)NC(CC(=O)N)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCSC)C(=O)NC(CCCCN)C(=O)NC(CC4=CNC5=CC=CC=C54)C(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(C(C)O)C(=O)NC(C)C(=O)NC(CC(C)C)C(=O)NC(CC(=O)O)C(=O)NC(CC6=CNC7=CC=CC=C76)C(=O)NC(CO)C(=O)NC(CC8=CNC9=CC=CC=C98)C(=O)NC(CC(C)C)C(=O)NC(CCC(=O)N)C(=O)NC(C(C)O)C(=O)NC(CCC(=O)O)C(=O)O)NC(=O)C(CCC(=O)N)NC(=O)C(CCCNC(=N)N)NC(=O)C(CC(=O)O)N

1. Systemic delivery of NEMO binding domain/IKKγ inhibitory peptide to young mdx mice improves dystrophic skeletal muscle histopathology

Daniel P Reay, Michele Yang, Jon F Watchko, Molly Daood, Terrence L O'Day, Khaleel K Rehman, Denis C Guttridge, Paul D Robbins, Paula R Clemens Neurobiol Dis. 2011 Sep;43(3):598-608. doi: 10.1016/j.nbd.2011.05.008. Epub 2011 May 23.

The activation of nuclear factor κB (NF-κB) contributes to muscle degeneration that results from dystrophin deficiency in human Duchenne muscular dystrophy (DMD) and in the mdx mouse. In dystrophic muscle, NF-κB participates in inflammation and failure of muscle regeneration. Peptides containing the NF-κB Essential Modulator (NEMO) binding domain (NBD) disrupt the IκB kinase complex, thus blocking NF-κB activation. The NBD peptide, which is linked to a protein transduction domain to achieve in vivo peptide delivery to muscle tissue, was systemically delivered to mdx mice for 4 or 7 weeks to study NF-κB activation, histological changes in hind limb and diaphragm muscle and ex vivo function of diaphragm muscle. Decreased NF-κB activation, decreased necrosis and increased regeneration were observed in hind limb and diaphragm muscle in mdx mice treated systemically with NBD peptide, as compared to control mdx mice. NBD peptide treatment resulted in improved generation of specific force and greater resistance to lengthening activations in diaphragm muscle ex vivo. Together these data support the potential of NBD peptides for the treatment of DMD by modulating dystrophic pathways in muscle that are downstream of dystrophin deficiency.

2. Inhibition of IKK activation, through sequestering NEMO, blocks PMMA-induced osteoclastogenesis and calvarial inflammatory osteolysis

John C Clohisy, Yasuhiro Yamanaka, Roberta Faccio, Yousef Abu-Amer J Orthop Res. 2006 Jul;24(7):1358-65. doi: 10.1002/jor.20184.

Osteoclasts, the primary bone-resorbing cells, play a crucial role in periprosthetic bone loss in response to implant-derived wear debris. Differentiation and activation of osteoclasts at the implant-bone interface are fueled by elevated levels of locally secreted inflammatory cytokines that heighten the osteolytic response. Among these cytokines are members of the TNF superfamily, including TNF and RANKL, which primarily act through activation of the transcription factor NF-kappaB. Activation of NF-kappaB is required for osteoclast formation, and its inhibition hampers osteoclastogenesis and bone loss. Activation of NF-kappaB is permitted following its dissociation from the inhibitory protein IkappaBalpha, an event subsequent to phosphorylation of the latter protein by the upstream IkappaBalpha kinase (IKK) complex. Our recent findings show that attenuating IKK complex assembly, by using a short peptide termed NEMO-binding domain (NBD) peptide, that blocks binding of IKK2 and IKK1 to IKKgamma/NEMO, inhibits NF-kappaB activation, and arrests RANKL-induced osteoclastogenesis. In this study, we examined if NBD is capable of blocking inflammatory osteolysis by PMMA particles. Our findings indicate that NBD peptide inhibits PMMA-induced IKK2 and NF-kappaB activation. More importantly, this peptide potently arrests PMMA-stimulated osteoclastogenesis and alleviates PMMA-induced inflammatory and osteolytic responses in mice. Thus, NBD peptide is considered as a promising modality to regulate inflammatory osteolysis.