[Des-Arg10]-HOE I40, B1 Bradykinin Receptor Antagonist

Product Name: [Des-Arg10]-HOE I40, B1 Bradykinin Receptor Antagonist

Sequence One Letter Code: rRP-Hyp-G-Thi-S-(D-Tic)-Oic

Sequence Three Letter Code: H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-OH

Chemical Formula:C53H77N15O12S

Molecular Weight: 1148.3

Purity: 95%

Form: Lyophilized

Storage Conditions: - 20 °C

Research Area: Cardiovascular Disease Research

Source / Species: Human, mouse, rat

Conjugation: Unconjugated

Code Nacres: NA.26

Application: [Des-Arg10]-HOE I40 is a synthetic peptide antagonist with high selectivity for the inducible bradykinin B1 receptor. Unlike the constitutively expressed B2 receptor, B1 is upregulated under inflammatory and pathological conditions. By competitively inhibiting B1 receptor activation, this peptide enables selective interrogation of B1-mediated signaling pathways involved in nociception, vascular permeability, and inflammatory responses. It is widely applied in models of chronic inflammation, neuropathic pain, and cardiovascular dysfunction. The antagonist supports mechanistic studies aimed at distinguishing B1-specific effects from B2 receptor signaling and facilitates pharmacological evaluation of bradykinin pathway modulation in disease-relevant experimental systems.

Current Research: [Des-Arg10]-HOE I40 is a synthetic peptide antagonist with high selectivity for the inducible bradykinin B1 receptor (B1R). The bradykinin system comprises two principal G protein–coupled receptors: B2, which is constitutively expressed under physiological conditions, and B1, which is minimally expressed in healthy tissues but strongly upregulated in response to inflammation, tissue injury, infection, and oxidative stress. By competitively inhibiting B1 receptor activation, [Des-Arg10]-HOE I40 enables selective interrogation of B1-mediated signaling pathways without significantly affecting B2 receptor activity. Bradykinin Receptor Biology Bradykinin peptides are generated through the kallikrein–kinin system and act as potent mediators of vasodilation, pain sensitization, and inflammatory responses. While B2 receptors respond primarily to intact bradykinin and kallidin, B1 receptors preferentially recognize des-Arg metabolites produced by carboxypeptidase-mediated cleavage during inflammatory states. B1 receptor expression is induced by pro-inflammatory cytokines such as IL-1β and TNF-α and is regulated at the transcriptional level through NF-κB–dependent pathways. This inducible profile makes B1R particularly relevant in chronic inflammation and pathological conditions rather than acute physiological signaling. Mechanism of Antagonism [Des-Arg10]-HOE I40 functions as a competitive antagonist at the B1 receptor, blocking ligand binding and preventing receptor-mediated signal transduction. Activation of B1R typically engages G_q and G_i pathways, leading to phospholipase C activation, intracellular calcium mobilization, and downstream signaling through PKC, MAPK, and nitric oxide pathways. By inhibiting these cascades, the antagonist provides a controlled means to assess B1-specific contributions to inflammatory signaling, vascular permeability, and nociceptive sensitization. Importantly, selective inhibition enables differentiation between B1-mediated responses and those driven by B2 receptor activation. Applications in Inflammation and Pain Research B1 receptor signaling has been implicated in chronic inflammatory conditions and neuropathic pain states. In experimental models, upregulation of B1R correlates with sustained hyperalgesia and tissue edema. [Des-Arg10]-HOE I40 is widely used to: Evaluate B1-dependent nociceptive pathways Investigate inflammatory mediator release Study cytokine-induced receptor upregulation Analyze vascular permeability changes Distinguish chronic from acute kinin signaling In neuropathic pain models, B1 antagonism can attenuate mechanical and thermal hypersensitivity, supporting mechanistic exploration of inflammatory pain circuits. Cardiovascular and Vascular Research Beyond pain and inflammation, B1 receptor activation influences endothelial function and vascular tone under pathological conditions such as hypertension, ischemia-reperfusion injury, and diabetic vascular dysfunction. Selective blockade with [Des-Arg10]-HOE I40 supports investigation of B1R-mediated nitric oxide production, oxidative stress responses, and endothelial permeability changes. By isolating inducible receptor signaling, researchers can clarify how chronic inflammatory stimuli alter vascular reactivity and contribute to disease progression. Pharmacological Evaluation and Receptor Specificity Because B1 and B2 receptors share structural homology but differ in expression patterns and ligand selectivity, distinguishing receptor-specific effects is critical in bradykinin pathway research. [Des-Arg10]-HOE I40 facilitates: Competitive binding studies Functional antagonism assays Comparative analysis of B1 versus B2 signaling Evaluation of novel kinin pathway modulators Its defined peptide structure ensures reproducible pharmacological performance in both in vitro and in vivo systems. Experimental Advantages High selectivity for inducible B1 receptor Competitive inhibition of B1-mediated signaling Suitable for chronic inflammation models Enables discrimination between B1 and B2 receptor pathways Compatible with cellular and animal experimental systems Research Significance [Des-Arg10]-HOE I40 serves as a critical tool for dissecting the role of the inducible bradykinin B1 receptor in inflammatory and pathological contexts. By enabling selective inhibition of B1R signaling, it supports mechanistic studies in chronic inflammation, neuropathic pain, and cardiovascular dysfunction. Its application enhances understanding of kinin pathway regulation and informs pharmacological strategies targeting bradykinin-mediated disease processes.