KLKB1 Specific Neutra™ Antibody Products

Kallikrein B1 (KLKB1) is a glycoprotein involved in surface-dependent activation of inflammation, blood coagulation, fibrinolysis, and kinin generation. The plasma-presented preproprotein forms a non-covalent complex with kininogen, and its proteolytic processing by activated coagulation factor XII produces a serine protease. Specific gene mutations may lead to prekallikrein deficiency, associated with conditions such as congenital prekallikrein deficiency.

Its Gene ID: 3818, UniProtKB ID: P03952, and OMIM ID: 229000.

KLKB1 Related Pathways

In a condition of resting, KLKB1 emerges as the primary catalyst for kinin production within organs, including blood vessels, while the angiotensin I-converting enzyme/kininase II (ACE) takes on the pivotal role of kinin deactivation within the circulating system, present in both the endothelium and plasma. ACE and kallikrein, despite their kinin-centric functions, are associated with additional physiological effects, a fact more extensively documented for ACE, initially recognized as the angiotensin I-activating/angiotensin II-generating enzyme.

KLKB1 participates in flow-induced vasodilatation, which is synthesized in Arteries. The synthesis of endothelial ACE exhibits a robust specificity toward vessels and organs, influencing the local bioavailability of angiotensins and kinins. In scenarios marked by pathological conditions arising from hemodynamic, ischemic, or metabolic challenges to the cardiovascular system and the kidneys, KLKB1 and kinins play a pivotal role in safeguarding end organs.

Fig.1 Interplay between the renin-angiotensin and kallikrein-kinin systems in physiological contexts.¹

Harness the Therapeutic Potential of Anti-KLKB1 Antibodies for Various Diseases

Anti-KLKB1 antibodies have multifaceted potential, such as prowess in addressing acute episodes of hereditary angioedema (HAE), safeguarding against thrombosis in KLKB1-deleted mice, and mitigating sterile chemical-induced inflammation.

• Anti-KLKB1 Antibodies in HAE and Beyond may Unleash Therapeutic Potential

KLKB1 assumes a pivotal role in the onset of acute episodes in HAE. In contrast to C1 inhibitor, KLKB1 experiences a decline in levels during HAE attacks, leading to the cleavage of high-molecular-weight kininogen. The resultant liberation of bradykinin, a key biologic peptide, is the primary driver of edema. KLKB1, along with its enzyme PKa, emerges as a central focus in HAE, presenting ample opportunities to enhance both acute and chronic HAE management. The therapeutic potential of anti-KLKB1 antibodies in HAE is noteworthy.

Fig.2 Physiological mechanisms safeguarding against thrombosis in mice with KLKB1 (PK) deletion.²

• Anti-KLKB1 Antibodies in Sterile Chemical Inflammation

KLKB1 might play an additional role in the realm of inflammation. Within the context of granulomatous enterocolitis induced by peptidoglycan-polysaccharide polymer, the PKa/kinin system activates to produce cHK. A recent development involves a monoclonal antibody targeting KLKB1, which effectively hinders the synovial recruitment of endothelial cell progenitors and mitigates the hyperproliferation of synovial cells in a rodent model of peptidoglycan-polysaccharide polymer-induced arthritis. Notably, mice with a combined knockout of HK (Kgn1) and klkb1 exhibit diminished swelling and reduced severity of joint arthritis, coupled with lower levels of inflammatory cytokines in a rodent serum transfer-induced arthritis model.

Creative Biolabs offers a diverse selection of anti-KLKB1 antibody products, engineered using recombinant techniques. Additionally, customization options are available for crafting KLKB1-based blocking or neutralizing antibodies to meet specific needs.

REFERENCES

1. Alhenc-Gelas, Francois, Nadine Bouby, and Jean-Pierre Girolami. "Kallikrein/K1, kinins, and ACE/kininase II in homeostasis and in disease insight from human and experimental genetic studies, therapeutic implication." Frontiers in Medicine 6 (2019): 136.
2. Schmaier, Alvin H. "Plasma prekallikrein: its role in hereditary angioedema and health and disease." Frontiers in Medicine 5 (2018): 3.