Synonym |
GPRP-NH2 |
Species |
Human |
Protein Accession |
N/A |
Purity |
Greater than 95% as determined by RP-HPLC and SDS-PAGE. |
Endotoxin Level |
Less than 1 EU/μg. |
Biological Activity |
N/A |
Expression System |
Chemical Synthesis |
Fusion Tag |
None |
Predicted Molecular Mass |
418.5 Da |
Formulation |
Lyophilized from a 0.2 μm filtered solution in Acetonitrile and Water with TFA. |
Reconstitution |
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml.
|
Storage & Stability |
Store at -20°C upon receipt, aliquot and store at -20°C or -80°C. Avoid repeated freeze-thaw
cycles. |
FAQ
What is GPRP-NH2 and how does it work?
GPRP-NH2 is a compound derived from the peptide sequence
Gly-Pro-Arg-Pro (GPRP), which is related to fibrin and plays a significant role in the body's
coagulation process. It functions as an antagonist to the polymerization of fibrin, which is a key
factor in blood clot formation. Fibrinogen is a soluble plasma protein that is converted into insoluble
fibrin threads in the clotting process. This conversion is critical as it helps form the structural
basis of a blood clot. When thrombin cleaves fibrinogen, fibrin monomers are produced, which then
polymerize to form a clot. GPRP-NH2 is designed to bind to the same sites on fibrin(ogen) that are
targeted during polymerization, thus preventing the formation of the fibrin meshwork. This mechanism can
be crucial in medical situations requiring the disruption of abnormal clot formation using its unique
capability of blocking fibrin polymerization without affecting the upstream coagulation cascade or
thrombin activity directly. This quality is particularly useful for therapeutic applications where
precise control over clot formation is necessary, such as in thrombosis management, without facing the
broader anticoagulant effects that come with typical anticoagulant drugs. By intervening at the level of
fibrin polymerization, GPRP-NH2 provides a targeted approach that can mitigate the risk of bleeding
associated with more systemic anticoagulation therapies.
Is GPRP-NH2 application restricted to
specific medical conditions?
Although originally researched for purposes related to coagulation
and thrombosis, the applications of GPRP-NH2 could be wide-ranging due to its unique mechanism of
modulating fibrin polymerization. In thrombosis, GPRP-NH2 can potentially serve as a therapeutic agent
to prevent pathological blood clot formation, offering an option for patients at risk of deep vein
thrombosis, pulmonary embolism, or stroke by interfering specifically with fibrin assembly rather than
thrombin activity. Beyond thrombosis, there is potential in surgical settings where manipulating clot
dynamics can reduce complications. For example, in cardiac surgeries or other procedures where blood
flow needs to be delicately managed, GPRP-NH2 could serve as an adjunct to maintain fluidity and address
clot-related complications by ensuring that excessive clot formation does not occur. Additionally, since
fibrin is involved in wound healing and tissue repair, GPRP-NH2 might influence the healing process in
injuries or post-operative conditions. There is increasing interest in investigating how modulating
fibrin networks could impact fibrotic diseases, where inappropriate fibrin deposition plays a role in
pathological fibrosis. Research may also explore its implications in cancer metastasis, as fibrin matrix
provides scaffolding for tumor cells to anchor and migrate. By interfering with fibrin's structural
properties, GPRP-NH2 could offer a method to impact tumor cell dissemination, potentially contributing
to cancer therapies aimed at hindrance of metastasis. These broad possibilities demonstrate that, while
initially designed for coagulation-related issues, GPRP-NH2 encapsulates a wider promise for
applications across various medical conditions.
How does the specificity of GPRP-NH2’s action
enhance its therapeutic potential?
The therapeutic potential of GPRP-NH2 is notably enhanced by
its high specificity towards fibrin polymerization. Unlike conventional anticoagulants which broadly
inhibit elements of the coagulation cascade, GPRP-NH2 precisely targets the final steps of
coagulation—the polymerization of fibrin threads. This specificity limits the interaction with upstream
processes such as platelet activation and thrombin generation, which are critical for normal hemostatic
function. As a result, therapies involving GPRP-NH2 are less likely to produce complications related to
excessive anticoagulation, such as bleeding. This specificity can allow patients to undergo treatment
without the accompanying risk of hemorrhage that often restricts the use of anticoagulants in clinical
practice, especially in scenarios requiring a fine balance between preventing clot formation and
maintaining normal blood clotting. Furthermore, the focused action of GPRP-NH2 enhances its utility in
contexts where systemic anticoagulation is undesirable or contraindicated, such as in patients with
contraindications to traditional anticoagulants due to high bleeding risk markers, or in surgeries where
localized control of clotting is preferred to avoid surgical site bleeds. Additionally, GPRP-NH2's
selective action on fibrin polymerization allows it to be considered in conjunction with other therapies
targeting different parts of the coagulation pathway. This opens opportunities for combination therapies
where the multifaceted nature of clotting disorders can be addressed through a synergistic approach,
enhancing therapeutic outcomes while minimizing side effects. Its specific nature thus not only broadens
the range of its safe application but also supports a more personalized therapy approach, tailoring
treatments to individual patient needs and profiles, a critical aspect of modern precision
medicine.
In what ways could GPRP-NH2 influence future research in hemostasis and
thrombosis?
GPRP-NH2 represents an innovative approach to managing and understanding hemostasis
and thrombosis, and it could stimulate advancements in several areas of research. Its ability to
interrupt fibrin mesh formation without affecting other aspects of coagulation can lead to dramatic
shifts in how researchers understand and handle blood clotting disorders. Historically, most
anticoagulation research has focused on agents that act upstream—namely on thrombin and other clotting
factors—which entail broader systemic effects and considerable hemorrhagic risks. The unique targeting
model of GPRP-NH2 could inspire the exploration and development of novel anticoagulants that exhibit
similar specificity, leading to therapeutics that exert minimal adverse effects while maintaining
efficacy. Furthermore, GPRP-NH2 could play a pivotal role in decoding the complexity of fibrin networks,
hence contributing to a deeper comprehension of thrombosis mechanisms and potentially unveiling new
pathways amenable to therapeutic intervention. In addition, research inspired by GPRP-NH2’s mechanism of
action could expand into the field of biomaterials, particularly in developing coatings or materials
geared for surgeries and wound care, where controlled blood clotting and tissue regeneration are key.
The emerging field of regenerative medicine could also benefit, as GPRP-NH2 could be implicated in
forming scaffolds that encourage cell growth and repair without excessive clotting. Moreover, advances
may be made in diagnostics measures, where its involvement in fibrin’s structural configuration might
turn into a tool for analyzing clot stability, helping assess patient risks more accurately. In summary,
GPRP-NH2 not only holds therapeutic potential but is likely to fuel a wealth of scientific inquiry,
shaping future understanding and treatment of coagulation-related conditions.
What are the
possible side effects associated with GPRP-NH2?
When exploring compounds with significant impacts
on hemostasis, understanding potential side effects is crucial, although specific side effects of
GPRP-NH2 have yet to be fully elucidated due to its place within recent biomedical research. The primary
concern with anticoagulants is invariably the risk of bleeding, which occurs when clot formation is
excessively hindered beyond safe or necessary limits. This risk is mitigated with GPRP-NH2 due to its
precise mode of action on fibrin formation instead of acting on other components of the clotting
cascade; however, thorough research is essential to assess the degree of this benefit. Hypothetically,
if administered in excessive amounts, even a targeted approach might contribute to bleeding issues,
especially in patients with underlying hemostatic fragility or concurrent use of other anticoagulants.
Attention must also be paid to potential hypersensitivity or allergic reactions resulting from its
peptide-based nature, as the immune response might be triggered in some individuals. In rare cases,
peptide drugs have led to immune-mediated infusion reactions or developed antibodies that neutralize the
drug or trigger allergic responses. Beyond this, potential interactions with other therapeutic drugs are
another consideration, which necessitates comprehensive studies on pharmacodynamics and
pharmacokinetics. It’s also possible that interference with fibrin polymerization could, under certain
conditions, affect processes unrelated to thrombotic events—such as wound healing—where fibrin's
scaffolding role is essential. New therapies are often accompanied by a learning curve in determining
their long-term safety and full side effect profiles, necessitating vigilant clinical trials and patient
monitoring routines during the initial introduction periods of GPRP-NH2 into therapeutic use. Only
rigorous clinical evaluation can eventually define the complete safety profile of such innovative
therapies, ensuring safe implementation in modern medicine.