Results 51 to 60 of about 19,166 (184)

Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model of Escherichia coli sepsis [PDF]

open access: yes, 2017
Bacterial sepsis triggers robust activation of the complement system with subsequent generation of anaphylatoxins (C3a, C5a) and the terminal complement complex (TCC) that together contribute to organ failure and death.
Popescu, Narcis Ioan   +19 more
core   +1 more source

Structural basis for therapeutic inhibition of complement C5.

open access: yes, 2016
Activation of complement C5 generates the potent anaphylatoxin C5a and leads to pathogen lysis, inflammation and cell damage. The therapeutic potential of C5 inhibition has been demonstrated by eculizumab, one of the world's most expensive drugs. However,
Elmlund, H   +23 more
core   +1 more source

Targeted management of coexistent severe thrombophilias—A case report of a successful pregnancy despite paroxysmal nocturnal hemoglobinuria and hereditary protein C deficiency

open access: yeseJHaem
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematological disorder characterized by the absence of complement regulatory proteins on the surface of erythrocytes, leading to intravascular hemolysis and thrombosis.
Julien Dereme   +5 more
doaj   +1 more source

Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies

open access: yesBlood Advances, 2018
: The complement and coagulation cascades interact at multiple levels in thrombosis and inflammatory diseases. In venous thrombosis, complement factor 3 (C3) is crucial for platelet and tissue factor (TF) procoagulant activation dependent on protein ...
Nadine Müller-Calleja   +5 more
doaj   +1 more source

Clinical Utility and Potential Cost Savings of Pharmacologic Monitoring of Eculizumab for Complement-Mediated Thrombotic Microangiopathy

open access: yesMayo Clinic Proceedings: Innovations, Quality & Outcomes, 2022
One of the treatment options for complement-mediated thrombotic microangiopathy (CM-TMA), also known as atypical hemolytic uremic syndrome, is the administration of the C5 complement inhibitor eculizumab.
Meera Sridharan, MD, PhD   +2 more
doaj   +1 more source

Incomplete inhibition by eculizumab: mechanistic evidence for residual C5 activity during strong complement activation

open access: yes, 2017
Eculizumab inhibits the terminal, lytic pathway of complement by blocking the activation of the complement protein C5 and shows remarkable clinical benefits in certain complement-mediated diseases.
Christoph Q. Schmidt   +23 more
core   +1 more source

Investigational drugs inhibiting complement for the treatment of geographic atrophy.

open access: yes, 2023
INTRODUCTION Geographic atrophy (GA) is a progressive form of age-related macular degeneration (AMD) that leads to severe visual impairment and central vision loss.
Ferro Desideri, Lorenzo   +6 more
core   +1 more source

Zilucoplan, a macrocyclic peptide inhibitor of human complement component 5, uses a dual mode of action to prevent terminal complement pathway activation

open access: yesFrontiers in Immunology, 2023
IntroductionThe complement system is a key component of the innate immune system, and its aberrant activation underlies the pathophysiology of various diseases.
Guo-Qing Tang   +14 more
doaj   +1 more source

Structure and influence of tick complement inhibitor on human complement component 5

open access: yes, 2008
To provide insight into the structural and functional properties of human complement component 5 (C5), we determined its crystal structure at a resolution of 3.1 Å.
Pietro Roversi   +34 more
core   +1 more source

Simultaneous C5 and CD14 inhibition limits inflammation and organ dysfunction in pig polytrauma

open access: yesFrontiers in Immunology, 2022
Dysfunctional complement activation and Toll-like receptor signaling immediately after trauma are associated with development of trauma-induced coagulopathy and multiple organ dysfunction syndrome.
Ludmila Lupu   +17 more
doaj   +1 more source

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