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Bradykinin (BK), which has the amino acid sequence Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg, is a crucial growth factor for prostate and small-cell lung cancer (PC). These tumors express receptors for many neuropeptides and have neuroendocrine-derived cells. Almost all lung cancer cell lines and many PC cells have BK receptors. There are two recognized classes of BK receptors. Most cells and organs express B2 receptors on a constant basis, which mediates BK's typical regulatory actions. Inflammation causes the production of B1 receptors, which are ordinarily absent. These receptors react to BK(1-8) (desArg9-BK) rather than BK.

With years of experience in the field of drug discovery and development, Creative Biolabs can offer bradykinin family drug discovery assays and products to contribute to the success of your project:

Overview of Bradykinin Receptor

Numerous studies have shown that the B1R may influence various neuropathic pain-related factors. For instance, a non-peptide B1R antagonist was able to reduce thermal hyperalgesia at day 21 in the partial sciatic nerve ligation (PSNL) model of neuropathic pain but had no impact on touch or cold allodynia. The B1R is also thought to play a role in the emergence of the hyperalgesia linked to diabetes. In a rat model of chemotherapy-induced neuropathy, B1R antagonists have been demonstrated to be antihyperalgesic. The inhibition of B1R expression on dorsal horn nerve terminals or intrinsic spinal cord neurons may be the cause of the interruption of pain signaling by B1R antagonists.

B2R is an important pharmacological target for the treatment of edema and pain symptoms and for maintaining the homeostasis of the cardiovascular system. The powerful B2R-selective agonist labradimil (Arg-Pro-Hyp-Gly-Thi-Ser ProTyr(Me)-psi(CH2NH)-Arg) is capable of temporarily increasing the permeability of the blood brain barrier (BBB) in the RG2 rat model of glioma, facilitating the entry of chemotherapeutics into the CNS to kill tumors in the brain. This is possible because the alteration of the vasculature around tumors, which limits drug delivery to the tumor interstitium, as well as the release of prostaglandin E2 and nitric oxide, which alter the vascular physiology and morphology, are the processes driving this phenomenon.

Bradykinin Receptor Drug Discovery

With the binding of B1 and B2 receptors, bradykinin produces strong effects in various pathophysiological conditions. The effects of bradykinin, for instance, are powerfully antihypertensive, antithrombogenic, antiproliferative, and antifibrogenic, to name a few. Bradykinin also plays a role in the inflammatory process by promoting vasodilation and increased vascular permeability by activating endothelial cells, which results in the usual signs of inflammation as redness, heat, swelling, and pain. As an example, bradykinin-dependent angioedema can be caused by hereditary or acquired C1-INH deficiency or the use of ACE inhibitors (ACEi) to treat hypertension, heart failure, diabetes, or scleroderma. Bradykinin specifically contributes to tissue hyper-responsiveness and local inflammation in allergic rhinitis, asthma, and anaphylaxis.


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