Kallidin - 342-10-9

Kallidin

Catalog Number: EVT-242164
CAS Number: 342-10-9
Molecular Formula: C56H85N17O12
Molecular Weight: 1188.4 g/mol
The product is for non-human research only. Not for therapeutic or veterinary use.

Product Introduction

Description

Kallidin, also known as lysyl-bradykinin, is a kinin peptide that plays a significant role in various physiological and pathological processes. It is a product of the kallikrein-kinin system, which is involved in inflammation, blood pressure regulation, pain, and other critical functions. Kallidin exerts its effects by interacting with specific cell surface receptors, primarily the bradykinin B2 receptor, leading to a cascade of biological responses1568.

Applications in Various Fields

Asthma and Respiratory Function

In asthmatic subjects, kallidin has been shown to provoke potent bronchoconstriction when inhaled, suggesting a role in the pathogenesis of bronchial asthma. This effect is thought to be mediated by the B2 receptors, as evidenced by cross-tachyphylactic studies demonstrating reduced airway response to kallidin following exposure to bradykinin1.

Stroke and Neuroprotection

Kallidinogenase, an enzyme that produces kallidin, has been studied for its neuroprotective effects in cerebral ischemia. In a mouse model of middle cerebral artery occlusion, human urinary kallidinogenase (HUK) treatment resulted in improved neurological function, reduced infarct size, and suppressed inflammation. The mechanism involves the inhibition of the nuclear factor-kappa B (NF-κB) pathway and activation of the MAPK/ERK pathway, highlighting the potential therapeutic application of kallidinogenase in stroke2.

Ocular Health

In the context of retinal vein occlusion (RVO), kallidinogenase has been used to reduce retinal edema and the size of non-perfused areas. The treatment increases blood flow and promotes the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), suggesting an Akt/eNOS-dependent mechanism. These findings support the use of kallidinogenase as a therapeutic agent for RVO patients3.

Cardiovascular System

Kallidin, along with bradykinin, has been found to increase myocardial blood flow and reduce myocardial vascular resistance. This vasodilatory effect is dose-dependent and demonstrates the sensitivity of the myocardial vascular bed to kallidin. However, in contrast to bradykinin, kallidin does not seem to stimulate metabolic heat production in the myocardium, indicating a difference in their effects on myocardial metabolism4.

Dermatology

The role of kallidin in skin inflammation has been explored in both normal and psoriatic subjects. Intradermal injections of kallidin induce weal and flare responses, which are key features of inflammation. The comparison of these responses between normal individuals and patients with psoriasis could provide insights into the involvement of kinins in psoriatic pathology7.

Renal Physiology

The kallikrein-kinin system, of which kallidin is a part, is known to be intimately involved in renal function. Kallidin acts as a potent stimulus for renal biochemical and physiological events, and abnormalities in the system have been associated with renal pathologies. The system's sensitivity to drugs affecting renal function further underscores its significance in renal physiology6.

Properties

CAS Number

342-10-9

Product Name

Kallidin

IUPAC Name

(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[2-[[(2S)-1-[(2S)-1-[(2S)-2-[[(2S)-2,6-diaminohexanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]amino]acetyl]amino]-3-phenylpropanoyl]amino]-3-hydroxypropanoyl]pyrrolidine-2-carbonyl]amino]-3-phenylpropanoyl]amino]-5-(diaminomethylideneamino)pentanoic acid

Molecular Formula

C56H85N17O12

Molecular Weight

1188.4 g/mol

InChI

InChI=1S/C56H85N17O12/c57-24-8-7-18-36(58)46(76)67-37(19-9-25-63-55(59)60)51(81)73-29-13-23-44(73)53(83)72-28-11-21-42(72)49(79)65-32-45(75)66-39(30-34-14-3-1-4-15-34)47(77)70-41(33-74)52(82)71-27-12-22-43(71)50(80)69-40(31-35-16-5-2-6-17-35)48(78)68-38(54(84)85)20-10-26-64-56(61)62/h1-6,14-17,36-44,74H,7-13,18-33,57-58H2,(H,65,79)(H,66,75)(H,67,76)(H,68,78)(H,69,80)(H,70,77)(H,84,85)(H4,59,60,63)(H4,61,62,64)/t36-,37-,38-,39-,40-,41-,42-,43-,44-/m0/s1

InChI Key

FYSKZKQBTVLYEQ-FSLKYBNLSA-N

SMILES

C1CC(N(C1)C(=O)C2CCCN2C(=O)C(CCCN=C(N)N)NC(=O)C(CCCCN)N)C(=O)NCC(=O)NC(CC3=CC=CC=C3)C(=O)NC(CO)C(=O)N4CCCC4C(=O)NC(CC5=CC=CC=C5)C(=O)NC(CCCN=C(N)N)C(=O)O

Synonyms

Bradykinin, Lysine
Bradykinin, Lysyl
Kallidin
Kallidin Tetraacetate
Kallidin, (D)-Isomer
Lys Bradykinin
Lys-Bradykinin
Lysine Bradykinin
Lysyl Bradykinin
N2 L Lysylbradykinin
N2-L-Lysylbradykinin
Tetraacetate, Kallidin

Canonical SMILES

C1CC(N(C1)C(=O)C2CCCN2C(=O)C(CCCN=C(N)N)NC(=O)C(CCCCN)N)C(=O)NCC(=O)NC(CC3=CC=CC=C3)C(=O)NC(CO)C(=O)N4CCCC4C(=O)NC(CC5=CC=CC=C5)C(=O)NC(CCCN=C(N)N)C(=O)O

Isomeric SMILES

C1C[C@H](N(C1)C(=O)[C@@H]2CCCN2C(=O)[C@H](CCCN=C(N)N)NC(=O)[C@H](CCCCN)N)C(=O)NCC(=O)N[C@@H](CC3=CC=CC=C3)C(=O)N[C@@H](CO)C(=O)N4CCC[C@H]4C(=O)N[C@@H](CC5=CC=CC=C5)C(=O)N[C@@H](CCCN=C(N)N)C(=O)O
Mechanism of Action

Kallidin mediates its effects through the activation of the bradykinin B2 receptor, which is a G protein-coupled receptor. Upon binding to this receptor, kallidin triggers a series of intracellular signaling pathways, including the phosphoinositide pathway, leading to the production of inositol phosphates and diacylglycerol. This results in the release of calcium from intracellular stores and the activation of protein kinase C (PKC). The activation of these signaling pathways can lead to various physiological responses, such as vasodilation, increased vascular permeability, and stimulation of inflammatory mediators58.

Interestingly, kallidin can also be directly activated by serine proteases such as kallikreins, which suggests a unique mechanism of receptor activation that is independent of its release from kininogens. This direct activation does not involve cross-desensitization with bradykinin, indicating a distinct pathway of action8.

Method of Synthesis or Extraction
Kallidin can be synthesized chemically or extracted from biological sources. Chemical synthesis involves the stepwise assembly of amino acids using solid-phase peptide synthesis. The yield and efficiency of chemical synthesis depend on the complexity of the peptide sequence and the purity of the starting materials. The environmental impact of chemical synthesis is minimal, but safety considerations must be taken into account when handling hazardous chemicals.
Extraction of kallidin from biological sources involves the isolation of kininogen from plasma or other biological fluids, followed by enzymatic cleavage using kallikrein enzymes. The yield and efficiency of extraction depend on the purity and concentration of kininogen and the activity of kallikrein enzymes. The environmental impact of extraction methods is minimal, but safety considerations must be taken into account when handling biological fluids.
Chemical Structure and Biological Activity
Kallidin is a nonapeptide with the sequence H-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-OH. It is structurally similar to bradykinin, another member of the kinin family of peptides. Kallidin binds to the B1 and B2 receptors, which are G protein-coupled receptors expressed on various cell types, including endothelial cells, smooth muscle cells, and immune cells.
Kallidin is a potent vasodilator and increases blood flow to tissues by relaxing vascular smooth muscle cells. It also increases vascular permeability and promotes the extravasation of immune cells to sites of inflammation. Kallidin is involved in the modulation of pain perception and can induce hyperalgesia in animal models. It also has pro-inflammatory effects and is involved in the regulation of immune responses.
Biological Effects
Kallidin has diverse effects on cell function and signal transduction. It activates various intracellular signaling pathways, including the phospholipase C, protein kinase C, and mitogen-activated protein kinase pathways. Kallidin also activates the nuclear factor-kappa B pathway, which is involved in the regulation of immune responses and inflammation.
Kallidin has potential therapeutic and toxic effects. It has been studied as a potential treatment for hypertension, inflammation, and pain. However, its clinical use is limited by its short half-life and rapid degradation by peptidases. Kallidin can also induce adverse effects, such as hypotension, edema, and bronchoconstriction.
Future Perspectives and Challenges
The use and study of kallidin face several limitations and challenges. The short half-life and rapid degradation of kallidin limit its clinical use as a therapeutic agent. The development of stable and selective kallidin receptor agonists and antagonists is needed to overcome this limitation. The environmental impact of kallidin on ecosystems and pollution management needs to be further studied to evaluate its potential risks and benefits. The safety considerations in the industrial use of kallidin need to be addressed to ensure the health and safety of workers and the environment.
Conclusion:
Kallidin is a peptide hormone with diverse biological effects and potential applications in medical, environmental, and industrial research. The synthesis and extraction methods, chemical structure, biological activity, and potential applications of kallidin have been discussed in this paper. The future perspectives and challenges in the use and study of kallidin have also been highlighted. Further research is needed to fully understand the role of kallidin in physiological processes and to develop safe and effective therapeutic agents based on its biological activity.

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