Bradykinin receptor B1 (B1R) (B1R)

The Bradykinin receptor B1 (B1R) is a G protein-coupled receptor that plays a central role in the kinin-kallikrein system, primarily mediating chronic inflammation and pain (UniProt P46663). Unlike the B2 receptor, which is constitutively expressed, B1R is typically induced in response to tissue injury or pro-inflammatory cytokines like IL-1β and TNF-α (NCBI Gene ID 623). It is specifically activated by 'generated kinins'—the carboxypeptidase-cleaved metabolites of bradykinin and kallidin, known as des-Arg9-bradykinin (DABK) and Lys-des-Arg9-bradykinin (LDABK) (IUPHAR/BPS Guide to Pharmacology). Activation of B1R leads to sustained vasodilation, increased vascular permeability, and the release of further inflammatory mediators. This signaling pathway contributes significantly to the pathogenesis of diabetic retinopathy, neuropathic pain, and rheumatoid arthritis (PubMed PMID: 15121017). Therapeutic development has focused on B1R antagonists, such as Anatibant and SSR-240612, to provide targeted anti-inflammatory and analgesic effects. These drugs aim to treat chronic conditions with a potentially superior safety profile compared to non-selective kinin inhibitors by targeting only the inducible receptor (PubMed PMID: 17110101). Research continues to explore its role in cardiovascular and renal protection, which may present challenges for long-term antagonism (PubMed PMID: 21114797).

Other names

BDKRB1B1 bradykinin receptorBradykinin B1 receptorKinin B1 receptorB1R

Antagonism of the B1 receptor to inhibit the pro-inflammatory and pro-nociceptive effects of its ligands, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin.