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Ac9-25

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Ac9-25 is a N-terminal peptide of Annexin I (AI/Lipocortin I) that inhibits leukocyte extravasation. It stimulates neutrophil NADPH oxidase activation by acting as a formyl peptide receptor 1 (FPR1) ligand.

Category

Peptide Inhibitors

Catalog number

BAT-016353

CAS number

284040-76-2

Molecular Formula

C99H143N23O33

Molecular Weight

2183.35

Specification
Reference Reading

IUPAC Name

(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-acetamido-5-amino-5-oxopentanoyl]amino]propanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-phenylpropanoyl]amino]-3-methylpentanoyl]amino]-4-carboxybutanoyl]amino]-4-amino-4-oxobutanoyl]amino]-4-carboxybutanoyl]amino]-4-carboxybutanoyl]amino]-5-amino-5-oxopentanoyl]amino]-4-carboxybutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-methylbutanoyl]amino]-5-amino-5-oxopentanoyl]amino]-3-hydroxybutanoyl]amino]-3-methylbutanoyl]amino]-6-aminohexanoic acid

Synonyms

L-Lysine, N2-acetyl-L-glutaminyl-L-alanyl-L-tryptophyl-L-phenylalanyl-L-isoleucyl-L-α-glutamyl-L-asparaginyl-L-α-glutamyl-L-α-glutamyl-L-glutaminyl-L-α-glutamyl-L-tyrosyl-L-valyl-L-glutaminyl-L-threonyl-L-valyl-; N2-Acetyl-L-glutaminyl-L-alanyl-L-tryptophyl-L-phenylalanyl-L-isoleucyl-L-α-glutamyl-L-asparaginyl-L-α-glutamyl-L-α-glutamyl-L-glutaminyl-L-α-glutamyl-L-tyrosyl-L-valyl-L-glutaminyl-L-threonyl-L-valyl-L-lysine; Ac-Gln-Ala-Trp-Phe-Ile-Glu-Asn-Glu-Glu-Gln-Glu-Tyr-Val-Gln-Thr-Val-Lys-OH

Purity

≥95%

Density

1.354±0.06 g/cm3

Boiling Point

2439.8±65.0°C at 760 mmHg

Sequence

Ac-QAWFIENEEQEYVQTVK

Storage

Store at -20°C

InChI

InChI=1S/C99H143N23O33/c1-10-49(6)81(121-94(149)67(42-53-18-12-11-13-19-53)117-91(146)69(44-55-46-105-58-21-15-14-20-57(55)58)115-83(138)50(7)106-84(139)59(107-52(9)124)27-34-71(101)126)97(152)113-65(33-40-78(136)137)89(144)118-70(45-74(104)129)92(147)111-63(31-38-76(132)133)87(142)109-62(30-37-75(130)131)86(141)108-60(28-35-72(102)127)85(140)110-64(32-39-77(134)135)88(143)116-68(43-54-23-25-56(125)26-24-54)93(148)119-79(47(2)3)95(150)112-61(29-36-73(103)128)90(145)122-82(51(8)123)98(153)120-80(48(4)5)96(151)114-66(99(154)155)22-16-17-41-100/h11-15,18-21,23-26,46-51,59-70,79-82,105,123,125H,10,16-17,22,27-45,100H2,1-9H3,(H2,101,126)(H2,102,127)(H2,103,128)(H2,104,129)(H,106,139)(H,107,124)(H,108,141)(H,109,142)(H,110,140)(H,111,147)(H,112,150)(H,113,152)(H,114,151)(H,115,138)(H,116,143)(H,117,146)(H,118,144)(H,119,148)(H,120,153)(H,121,149)(H,122,145)(H,130,131)(H,132,133)(H,134,135)(H,136,137)(H,154,155)/t49-,50-,51+,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,79-,80-,81-,82-/m0/s1

InChI Key

VWAGQOJTUDBVPD-ZONPJGGESA-N

Canonical SMILES

CCC(C)C(C(=O)NC(CCC(=O)O)C(=O)NC(CC(=O)N)C(=O)NC(CCC(=O)O)C(=O)NC(CCC(=O)O)C(=O)NC(CCC(=O)N)C(=O)NC(CCC(=O)O)C(=O)NC(CC1=CC=C(C=C1)O)C(=O)NC(C(C)C)C(=O)NC(CCC(=O)N)C(=O)NC(C(C)O)C(=O)NC(C(C)C)C(=O)NC(CCCCN)C(=O)O)NC(=O)C(CC2=CC=CC=C2)NC(=O)C(CC3=CNC4=CC=CC=C43)NC(=O)C(C)NC(=O)C(CCC(=O)N)NC(=O)C

1. Delayed shortening and shrinkage of cochlear outer hair cells

T Kumazawa, M Hara, M Inoue, T Yamashita, S Ohnishi, A Minato, C Inagaki Am J Physiol . 1992 Nov;263(5 Pt 1):C1088-95. doi: 10.1152/ajpcell.1992.263.5.C1088.

Slow shortening of cochlear outer hair cells has been speculated to modify cochlear sensitivity. Tetanic electrical field stimulation of isolated outer hair cells from guinea pigs shortened the cells for 2-3 min. Electrical stimulation reduced cell length and volume (-13.5 +/- 1.5 and -37.3 +/- 3.0% of initial values, respectively, n = 16) and decreased the intracellular Cl- concentration. Cytochalasin B (100 microM) inhibited electrical stimulation-induced shortening but not volume reduction. The following chemicals or manipulations inhibited the responses: 10 microM furosemide, 0.1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), 1 mM anthracene-9-carboxylic acid (AC9), 25 mM tetraethylammonium, 2.3 microM charybdotoxin (ChTX), 250 nM omega-conotoxin, and Ca(2+)-free medium. These findings suggest that both electrical stimulation-induced shortening and shrinkage of outer hair cells result not only from an actin-mediated contractile force, but also from Cl- efflux through furosemide-, DIDS-, and AC9-sensitive Cl- channels, and K+ efflux through ChTX-sensitive K+ channels.

2. Neutrophil NADPH-oxidase activation by an annexin AI peptide is transduced by the formyl peptide receptor (FPR), whereas an inhibitory signal is generated independently of the FPR family receptors

Kristoffer Hellstrand, Huamei Fu, Jennie Karlsson, Charlotta Movitz, François Boulay, Claes Dahlgren J Leukoc Biol . 2005 Sep;78(3):762-71. doi: 10.1189/jlb.0305153.

Truncation of the N-terminal part of the calcium-regulated and phospholipid-binding protein annexin AI has been shown to change the functional properties of the protein and to generate immunoregulatory peptides. Proinflammatory as well as anti-inflammatory signals are triggered by these peptides, and the two formyl peptide receptor (FPR) family members expressed in neutrophils, FPR and FPR-like 1 (FPRL1), have been suggested to transduce these signals. We now report that an annexin AI peptide (Ac9-25) activates, as well as inhibits, the neutrophil release of superoxide anions. Results obtained from experiments with receptor antagonists/inhibitors, desensitized cells, and transfected cells reveal that the Ac9-25 peptide activates the neutrophil reduced nicotinamide adenine dinucleotide phosphate oxidase through FPR but not through FPRL1. The Ac9-25 peptide also inhibits the oxidase activity in neutrophils triggered, not only by the FPR-specific agonist N-formyl-Met-Leu-Phe but also by several other agonists operating through different G protein-coupled receptors. Our data show that the two signals generated by the Ac9-25 peptide are transmitted through different receptors, the inhibitory signal being transduced by a not-yet identified receptor distinct from FPR and FPRL1.