Synonym |
Fibrinogen alpha chain |
Species |
Human |
Protein Accession |
P02671 |
Purity |
≥ 95% by HPLC |
Endotoxin Level |
< 1.0 EU per µg |
Biological Activity |
Not specified |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
7.1 kDa |
Formulation |
Lyophilized |
Reconstitution |
It is recommended to reconstitute the lyophilized Fibrinopeptide B in sterile 18MΩ-cm H2O not
less than 100µg/ml, which can then be further diluted to other aqueous solutions. |
Storage & Stability |
Store lyophilized Fibrinopeptide B at -20°C. Aliquot the product after reconstitution to avoid
repeated freezing/thawing cycles. Reconstituted product is stable for up to 12 months at -20°C.
|
FAQ
What is Fibrinopeptide B and how does it function in the body?
Fibrinopeptide B is a peptide
generated during the blood coagulation process. It is a fragment released when fibrinogen is cleaved to
form fibrin, a major structural component of a blood clot. The peptide plays an instrumental role in the
complex cascade of hemostatic reactions that occur following blood vessel injury. Understanding the
function of Fibrinopeptide B requires a basic comprehension of the coagulation process. When a blood
vessel is injured, the body initiates a series of interlinked enzymatic reactions collectively termed
the coagulation cascade. This cascade involves several clotting factors that ultimately transform
fibrinogen, a soluble plasma protein produced by the liver, into fibrin, an insoluble protein that
meshes together to form a stable clot.
Fibrinopeptide B is released from the B-beta chains of
fibrinogen during the thrombin-catalyzed conversion of fibrinogen to fibrin. Thrombin cleaves
fibrinogen, removing fibrinopeptides A and B, allowing the fibrin monomers to polymerize and form a
fibrin clot. This conversion is a pivotal step in hemostasis, as it effectively transforms fibrinogen
into a fibrin matrix that traps blood cells, thereby stabilizing the initial plug formed at the wound
site.
Moreover, Fibrinopeptide B, along with its counterpart Fibrinopeptide A, serves as a
biomarker in clinical diagnostics not only for monitoring coagulation disorders but also for evaluating
the activation of the coagulation system in various diseases. Elevated levels of Fibrinopeptide B can
indicate excessive thrombin activity, such as in disseminated intravascular coagulation or during severe
inflammatory responses. Furthermore, recent research suggests that these peptides may have roles beyond
coagulation, for example, in modulating inflammation and cellular signaling pathways involving other
proteins and receptors. The ability of Fibrinopeptide B to interact with specific cellular receptors
hints at its potential involvement in additional biological processes, though these roles are still
under investigation.
What are the clinical implications of abnormal Fibrinopeptide B
levels?
Abnormal levels of Fibrinopeptide B in clinical settings can indicate various
pathological conditions related to coagulatory dysfunction. Elevated levels often reflect excessive
thrombin activity and resultant fibrin formation, while lower or irregular levels can signal
deficiencies in clotting potential, pointing healthcare providers to several potential health issues.
Increased Fibrinopeptide B levels are often associated with thrombotic disorders, where there is a
propensity for unwanted clot formation. This can include deep vein thrombosis (DVT), pulmonary embolism
(PE), and other conditions characterized by abnormal clot formation in the bloodstream. Raised levels
may also be observed in acute inflammatory conditions and severe infections like sepsis, where
coagulation and inflammation pathways are simultaneously activated in response to infection or
injury.
On the opposite spectrum, insufficient levels or production of Fibrinopeptide B can
indicate bleeding disorders. Conditions such as liver disease, which can impair the synthesis of
coagulation factors like fibrinogen, can manifest as lowered production of Fibrinopeptide B and parallel
a compromised ability to form stable clots. Disorders like hemophilia, although directly related to
deficiencies in specific clotting factors, can also reflect in altered levels of fibrinopeptides due to
impacted downstream coagulation processes.
Besides indicating these disorders, Fibrinopeptide B
levels can inform about the efficacy of anticoagulant therapies. Monitoring these levels assists
clinicians in adjusting therapeutic strategies for conditions requiring anticoagulation, such as atrial
fibrillation or mechanical heart valve replacements, ensuring that the delicate balance between
preventing clot formation and causing excessive bleeding is maintained. Additionally, research into
Fibrinopeptide B is providing deeper insights into the link between coagulation and inflammation.
Elevated levels can correlate with inflammatory diseases and conditions like rheumatoid arthritis, where
the interplay between coagulative and immune mechanisms contributes to disease progression. The
potential of Fibrinopeptide B as a therapeutic target is also gaining interest, given its emerging roles
in other body systems beyond hemostasis.
Can Fibrinopeptide B levels affect cardiovascular
health?
Fibrinopeptide B levels, as part of the broader hemostatic system, can have significant
implications for cardiovascular health. Cardiovascular diseases (CVD) are often associated with
aberrations in coagulation processes, and dysregulation of fibrinogen cleavage to fibrin, as indicated
by variations in Fibrinopeptide B levels, can be both a biomarker and a contributor to cardiovascular
pathologies. Elevated Fibrinopeptide B suggests increased thrombin activity, reflecting enhanced
coagulation potential and possibly hypercoagulability. This condition can lead to the formation of
arterial or venous thrombi, critical events in cardiovascular diseases. Thrombi can occlude blood
vessels or become embolic, leading to events like myocardial infarction (heart attack) or ischemic
stroke, which are leading causes of morbidity and mortality worldwide.
Furthermore, individuals
with elevated fibrinogen and correlatively, elevated Fibrinopeptide B levels, often exhibit a
pro-inflammatory state. Inflammation is a key factor in the pathogenesis of atherosclerosis, a principal
cause of CVD, where endothelial dysfunction and plaque formation in blood vessels are precipitated by
persistent inflammation and coagulation activity. Therefore, chronic elevation of Fibrinopeptide B may
also suggest active atherogenesis, where an increased clotting tendency exists alongside vascular
inflammation and oxidative stress that contribute to arterial plaque development.
In this
context, Fibrinopeptide B levels are not only relevant in acute cardiovascular events but can also
provide insights into more chronic conditions associated with arterial disease and complications.
Monitoring levels can aid in evaluating cardiovascular risk and the effectiveness of therapeutic
interventions, like lifestyle modifications, antiplatelet, or anticoagulant therapies. Emerging research
highlights the potential of targeting coagulation pathways, including fibrin and fibrinopeptide
pathways, to mitigate cardiovascular risks and treat CVD. This underscores the importance of optimizing
coagulation factor levels, including Fibrinopeptide B, as part of a holistic strategy to improve
cardiovascular outcomes and tailor them to individual patient profiles.
How can Fibrinopeptide B
serve as a biomarker for diseases?
As a by-product of fibrinogen cleavage, Fibrinopeptide B
serves as a crucial biomarker for various pathological states, particularly those involving coagulation
and inflammation. Its levels reflect thrombin activity, one of the terminal processes in blood
coagulation essential for clot formation. Thus, fluctuations in its levels act as significant indicators
of hemostatic balance or imbalance within the body. In clinical diagnostics, Fibrinopeptide B is
deployed for assessing activation of coagulation processes. For instance, in venous thromboembolism
(VTE) disorders such as deep vein thrombosis or pulmonary embolism, heightened levels can suggest
abnormal clotting activity, warranting further investigation or intervention.
Beyond coagulation,
Fibrinopeptide B provides insights into conditions characterized by inflammation. Chronic inflammatory
conditions, including autoimmune disorders like rheumatoid arthritis or systemic lupus erythematosus,
often exhibit elevated fibrinopeptide levels. This is because inflammatory processes can augment
thrombin generation and fibrinolysis, reflected in the measured concentrations of fibrinopeptides.
Monitoring these levels assists clinicians in evaluating disease activity, response to treatment, and
potential complications associated with thrombotic risk.
Moreover, Fibrinopeptide B is being
investigated as a biomarker in cancer diagnosis and prognosis. Thrombosis is increasingly recognized as
a common complication in cancer patients, categorized under the term Trousseau’s syndrome. Elevated
fibrinopeptide levels may not only indicate a predisposition to thrombosis in these patients but also
correlate with tumor progression, metastasis, and overall prognosis. The dual role of fibrinopeptides in
coagulation and immune system interplay makes them valuable tools for stratifying patient risk,
evaluating disease progression, and adjusting therapeutic approaches. As research advances,
understanding and utilizing Fibrinopeptide B as a biomarker could expand, offering comprehensive
insights across multiple diseases, refining diagnostics, and enhancing personalized medicine
strategies.
Are there any therapeutic uses of Fibrinopeptide B in modern medicine?
While
Fibrinopeptide B itself is not directly used as a therapeutic agent, its role and implications in the
hemostatic system make it a significant focal point for therapeutic research and development. Based on
its function in the coagulation cascade, as a product of fibrinogen cleavage, therapeutic strategies
often center on modulating the pathways involving fibrinopeptides to manage clotting disorders. In
anticoagulation therapy, understanding the dynamics of fibrinopeptides helps in the development of
agents that can more precisely control thrombin activity and fibrin formation, thereby preventing
excessive clot formation while avoiding bleeding risks. Agents such as direct thrombin inhibitors
utilize our understanding of fibrinogen cleavage and fibrinopeptide release to more finely tune
therapeutic outcomes.
Furthermore, given its relationship with inflammation, Fibrinopeptide B is
being studied for its role in inflammatory conditions, which may yield novel anti-inflammatory
therapies. Conditions such as rheumatoid arthritis or inflammatory bowel diseases, where the interplay
between coagulation and inflammation exacerbates disease pathology, could potentially benefit from
therapies targeting fibrinopeptide pathways. Such strategies might involve modulating receptor
interactions or reducing fibrinopeptide-mediated inflammatory signaling.
In oncology, where
coagulation and tumor biology intersect, targeting fibrinopeptide-modulated pathways offers a frontier
for therapeutic innovation. Anticoagulants are sometimes employed in cancer care, with ongoing studies
exploring how interventions affecting thrombin and fibrin processes can influence tumor growth and
metastasis. Here, fibrinopeptides become markers for disease state and therapy response, guiding the use
of existing therapies like low molecular weight heparins or advocating for new therapeutic
pipelines.
While not a direct therapeutic agent, the understanding of Fibrinopeptide B’s function
and impact across various biological systems facilitates the development of interventions leveraging its
role in coagulation and inflammation. This underscores the importance of ongoing research to elucidate
its protective and pathogenic roles and potentially unlock new therapeutic avenues targeting these
pathways, enhancing treatments for a variety of thrombo-inflammatory conditions and possibly others
where Fibrinopeptide B plays a modulatory role.