Substance P (1-7)

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Substance P (1-7)
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Substance P (1-7) is a fragment of Substance P (SP), and Substance P (SP) is an endogenous tachykinin neuropeptide.

Peptide Inhibitors
Catalog number
CAS number
Molecular Formula
Molecular Weight
Substance P (1-7)
2-[[5-amino-2-[[5-amino-2-[[1-[6-amino-2-[[1-[2-amino-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]hexanoyl]pyrrolidine-2-carbonyl]amino]-5-oxopentanoyl]amino]-5-oxopentanoyl]amino]-3-phenylpropanoic acid
Substance P Fragment 1-7
White Powder
≥97% by HPLC
1.49±0.1 g/cm3(Predicted)
Store at -20°C
InChI Key
Canonical SMILES
1. Small peptides mimicking substance P (1-7) and encompassing a C-terminal amide functionality
Anja Sandström, Milad Botros, Rebecca Fransson, Mathias Hallberg, Gunnar Lindeberg, Fred Nyberg Neuropeptides . 2008 Feb;42(1):31-7. doi: 10.1016/j.npep.2007.11.002.
Some of the biological effects demonstrated after administration of substance P (SP) in vivo can indirectly be attributed to the fragmentation of the undecapeptide to its N-terminal bioactive fragment SP(1-7). This heptapeptide (H-Arg-Pro-Lys-Pro-Gln-Gln-Phe-OH) is a major bioactive metabolite from SP that frequently exerts similar biological effects as the parent peptide but also, in several cases, completely opposite actions. Specific binding sites for the heptapeptide SP(1-7) that are separate from the SP preferred NK receptors have been identified. In this study we demonstrate that (a) the C-terminal part of the SP metabolite SP(1-7) is most important for binding as deduced from an Ala scan and that a replacement of Phe(7) for Ala is deleterious, (b) truncation of the N-terminal amino acid residues of SP(1-7) delivers peptides with retained binding activity, although with somewhat lower binding affinities than SP(1-7) and (c) a C-terminal amide group as a replacement for the terminal carboxy group of SP(1-7) and for all of the truncated ligands synthesized affords approximately 5-10-fold improvements of the binding affinities.
2. Impact of N-methylation of the substance P 1-7 amide on anti-allodynic effect in mice after peripheral administration
Anna Skogh, Anna Lesniak, Anja Sandström, Fabienne Z Gaugaz, Rebecca Fransson, Mathias Hallberg, Gunnar Lindeberg, Richard Svensson, Fred Nyberg Eur J Pharm Sci . 2017 Nov 15;109:533-540. doi: 10.1016/j.ejps.2017.09.007.
Substance P 1-7 (SP1-7, Arg1-Pro2-Lys3-Pro4-Gln5-Gln6-Phe7) is the major bioactive metabolite formed after proteolytic degradation of the tachykinin substance P (SP). This heptapeptide often opposes the effects of the mother peptide. Hence, SP1-7is having anti-inflammatory, anti-nociceptive and anti-hyperalgesic effects in experimental models. Despite all encouraging properties of SP1-7its exact mode of action has not yet been elucidated which has hampered further development of this heptapeptide in drug discovery. Contrary to SP that mediates its biological activity via the NK-1 receptor, the N-terminal fragment SP1-7acts through an unknown target that is distinct from all known opioid and tachykinin receptors. The SP1-7amide 1 (Arg1-Pro2-Lys3-Pro4-Gln5-Gln6-Phe7-NH2) was previously shown to be superior to the endogenous SP1-7in all experimental pain models where the two compounds were compared. Herein, we report that N-methylation scan of the backbone of the SP1-7amide (1) results in peptides that are significantly less prone to undergo proteolysis in plasma from both mouse and human. However, with the two exceptions of the [MeLys3]SP1-7amide (3) and the [MeGln5]SP1-7amide (4), the peptides with a methyl group attached to the backbone are devoid of significant anti-allodynic effects after peripheral administration in the spared nerve injury (SNI) mouse model of neuropathic pain. It is suggested that the N-methylation does not allow these peptides to form the accurate bioactive conformations or interactions required for efficient binding to the macromolecular target. The importance of intact N-terminal Arg1and C-terminal Phe7, anticipated to serve as address and message residues, respectively, for achieving the anti-allodynic effect is emphasized. Notably, the three heptapeptides: the SP1-7amide (1), the [MeLys3]SP1-7amide (3) amide and the [MeGln5]SP1-7amide (4) are all considerably more effective in the SNI mouse model than gabapentin that is widely used in the clinic for treatment of neuropathic pain.
3. Intrathecal substance P (1-7) prevents morphine-evoked spontaneous pain behavior via spinal NMDA-NO cascade
Hikari Kuwahata, Takaaki Komatsu, Chizuko Watanabe, Tsukasa Sakurada, Toru Orito, Chikai Sakurada, Shinobu Sakurada, Minoru Tsuzuki Biochem Pharmacol . 2007 Sep 1;74(5):758-67. doi: 10.1016/j.bcp.2007.05.025.
Previous research has shown that injection of high-dose of morphine into the spinal lumbar intrathecal (i.t.) space of rats elicits an excitatory behavioral syndrome indicative of severe vocalization and agitation. Substance P N-terminal fragments are known to inhibit nociceptive responses when injected i.t. into animals. In this study, we investigated the effect of i.t. substance P (1-7) on both the nociceptive response and the extracellular concentrations of glutamate and nitric oxide (NO) metabolites (nitrite/nitrate) evoked by high-dose i.t. morphine (500 nmol). The induced behavioral responses were attenuated dose-dependently by i.t. pretreatment with the substance P N-terminal fragment substance P (1-7) (100-400 pmol). The inhibitory effect of substance P (1-7) was reversed significantly by pretreatment with [d-Pro2, d-Phe7]substance P (1-7) (20 and 40 nmol), a d-isomer and antagonist of substance P (1-7). In vivo microdialysis analysis showed a significant elevation of extracellular glutamate and NO metabolites in the spinal cord after i.t. injection of high-dose morphine (500 nmol). Pretreatment with substance P (1-7) (400 pmol) produced a significant reduction on the elevated concentrations of glutamate and NO metabolites evoked by i.t. morphine. The reduced levels of glutamate and NO metabolites were significantly reversed by the substance P (1-7) antagonist (40 nmol). The present results suggest that i.t. substance P (1-7) may attenuate the excitatory behavior (vocalization and agitation) of high-dose i.t. morphine by inhibiting the presynaptic release of glutamate, and reducing NO production in the dorsal spinal cord.

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