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[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P, commonly called Antagonist D, is a modified Substance P analog developed as a broad-spectrum neuropeptide antagonist.
Its pharmacology extends beyond simple NK1 blockade. Published studies show inhibition of multiple neuropeptide signaling systems together with context-dependent agonist signaling, making Antagonist D a useful tool for studying ligand efficacy and GPCR cross-reactivity.
Product Information
| Product Name | [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P |
| Catalog No. | AS2537 |
| CAS No. | 96736-12-8 |
| Synonym | Antagonist D |
| Sequence | D-Arg-Pro-Lys-Pro-D-Phe-Gln-D-Trp-Phe-D-Trp-Leu-Leu-NH2 |
| Peptide Length | 11 residues |
| Molecular Formula | C79H109N19O12 |
| Molecular Weight | Approximately 1516.8 Da |
| Key Modifications | D-Arg1; D-Phe5; D-Trp7; D-Trp9; Leu11 |
| Research Profile | Broad-spectrum neuropeptide antagonist |
Broad-Spectrum GPCR Antagonism
Antagonist D has been shown to interfere with signaling initiated by several neuropeptides rather than acting exclusively at a single tachykinin receptor. Later work demonstrated interaction with additional GPCR families, including vasopressin-related receptor systems.
This broad pharmacology is useful experimentally but also means that inhibition should not automatically be interpreted as proof of NK1 involvement.
Antagonist D Can Also Produce Biased Signaling
An important non-commodity feature of this peptide is that antagonist behavior does not describe its entire pharmacology. At concentrations that inhibit neuropeptide-induced calcium signaling, Antagonist D has also been reported to activate JNK, induce cytoskeletal changes and stimulate responses in human neutrophils.
We therefore recommend measuring the downstream endpoint of interest rather than assuming that blockade of Ca2+ mobilization predicts complete receptor silence.
Metabolic Stability and the C-Terminus
Antagonist D showed less than 13% degradation over 24 hours at 37°C in water, 1 M acetic acid and plasma in one comparative stability study. Liver homogenate degradation occurred more rapidly, with a reported half-life of approximately 0.98 hours under the tested conditions.
Research Applications
Antagonist D can support broad-spectrum neuropeptide signaling research, GPCR cross-reactivity studies, biased agonism experiments, peptide metabolism studies and cancer-related neuropeptide signaling models.
Frequently Asked Questions
Is Antagonist D simply an NK1 antagonist?
No. Its published pharmacology includes broader neuropeptide receptor interactions.
Can Antagonist D produce agonist signaling?
Yes. Context-dependent JNK activation and other agonist-like responses have been reported despite antagonism of calcium signaling.
Does it contain methionine?
No. Met11 is replaced by Leu.