Staffed by dedicated scientists with combined knowledge and expertise in complement therapeutic research, Creative Biolabs providing a full range of complement therapeutic services for our customer. Based on our extensive knowledge, we are fully equipped to reach out to our clients who may have problem or difficulty dealing with Chemotherapy-induced Neutropenia drug development.
Chemotherapy-induced Neutropenia
The duration and degree of neutropenia determine the risk of infection. Neutrophils are the first line of defense against infection, the first cellular component of the inflammatory response and a key component of innate immunity. Chemotherapy makes cancer patients susceptible to infection by inhibiting the production of neutrophils and the cytotoxic effect of cells on the digestive tract. Neutropenia blunts the inflammatory response of neonatal infections, leading to the multiplication and invasion of bacteria. Since the neutropenia reduces the signs and symptoms of infection, the only sign of infection presented by patients with neutropenia is fever.
MASP-2
MASP-2 is an enzyme encoded by the MASP2 gene in humans and it participates in the complement system. MASP-2 shares a common ancestor with the C1s molecules of the classical complement pathway and is therefore very similar. When the carbohydrate recognition head of MBL binds to mannose residues specifically arranged on the surface of pathogens, MASP-2 is activated and cleaved complement components C4 and C2 into C4a, C4b, C2a, and C2b.
Fig.1 Schematic diagram of the proposed autoactivation mechanism of MASP-2. (Gál, 2005)
The Impact of MASP-2 Deficiency on Chemotherapy-induced Neutropenia
MASP-2 is an essential component of the complement-activated lectin pathway. Its deficiency is common due to genetic polymorphisms, but its impact on susceptibility to infection remains to be studied. MBL and ficolins both activate MASP-2, resulting in bacterial death by complement activation. The defect of the complement-activated lectin pathway is a major cause of innate immunity that occurs frequently due to polymorphisms and may affect individual susceptibility to infection. It has been proved that patients with cancer and MASP-2 deficiency develop more frequent or more severe episodes of fever and severe chemotherapy-induced neutropenia (FN).
As one of the most highly respected drug discovery and antibody development laboratories in the world, Creative Biolabs has been helping customers all over the world make fast and effective biotherapeutics development decisions for decades.
The advanced Complement Therapeutics Platform is equipped to offer a full range of biotherapeutics development services regarding drug discovery and validation for chemotherapy-induced neutropenia. Please feel free to contact us for detailed information.
Reference
1. Gál, P. A true autoactivating enzyme. Structural insight into mannose-binding lectin-associated serine protease-2 activations. J Biol Chem. 2005, 280(39), 33435-33444.
Related Product
Questions & Answer
A: The complement system, a part of the body's immune system, also gets activated during chemotherapy. However, excessive complement activation can contribute to chemotherapy-induced tissue damage, including neutropenia. Complement therapeutic strategies aim at inhibiting the complement system to reduce its harmful effects. It can potentially reduce the risk of chemotherapy-induced neutropenia.
A: Complement therapy involves using targeted agents to regulate or modulate the activity of the complement system. Available inhibitors target different parts of the complement system. They include C1 inhibitors, Factor B inhibitors, C3 inhibitors, C5 inhibitors, and C5a receptor antagonists. In the context of chemotherapy-induced neutropenia, complement therapy aims to mitigate neutropenia by enhancing immune responses and reducing the risk of infections. Complement therapy may help reduce the severity and duration of neutropenia, lower the risk of infections, and improve patients' overall quality of life during and after chemotherapy.
A: While specific agents may be under investigation, no single complement inhibitor or activator has been universally established for treating chemotherapy-induced neutropenia. Research is ongoing to identify effective candidates.
For Research Use Only.
Related Sections:
