CLINICAL TRIALS PROFILE FOR AMINOCAPROIC ACID

All Clinical Trials for aminocaproic acid

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00156520 ↗	Platelet Function And Aggregometry In Patients With Aortic Valve Stenosis	Completed	University of Rochester	Phase 4	2005-03-01	It is known that patients with aortic stenosis, including those undergoing cardiac surgery for this problem, are prone to developing bleeding problems, particularly of the gastrointestinal tract. It is believed that the shear stress associated with blood flow through the abnormal aortic valve results in abnormal hemostasis. Abnormalities include increased proteolysis of the von Willebrand factor (vWF) and increased binding of the high molecular weight multimers of vWF to platelet membranes with subsequent inappropriate platelet aggregation. Thus, appropriate aggregation of circulating platelets is impaired. Cardiac surgery is associated with significant alterations in hemostasis. Patients undergoing cardiac surgery consume a significant percent of available blood products throughout the United States and are subjected to various and numerous risks associated with blood product transfusion. In addition, excessive postoperative bleeding is a common cause for the need to surgically re-explore the chest cavity in patients who have just undergone cardiac surgical procedures. Such additional surgery carries further cost and risk. Following surgical correction of aortic valve stenotic pathology, associated vWF abnormalities appear to reverse. However, this process can take several days. Although all cardiac surgical patients are at risk for postoperative bleeding, patients undergoing aortic valve surgery for aortic stenosis may be particularly at risk for this postoperative complication. In addition, patients with aortic valve stenosis who undergo noncardiac surgery may have a predisposition to bleeding because of similar underlying shear stress induced abnormal vWF and platelet function. The proposed study is a trial to evaluate the effectiveness of 2 different antifibrinolytic drugs in ameliorating the hemostatic defect associated with aortic stenosis. Aprotonin, an antifibrinolytic agent which also has platelet preserving actions4, will be compared to the currently used anti-fibrinolytic, epsilon aminocaproic acid (EACA).
NCT00223704 ↗	Bradykinin Receptor Antagonism During Cardiopulmonary Bypass	Completed	Vanderbilt University	Phase 2/Phase 3	2006-05-01	Each year over a million patients worldwide undergo cardiac surgery requiring cardiopulmonary bypass (CPB). CPB is associated with significant morbidity including the transfusion of allogenic blood products, inflammation and hemodynamic instability. In fact, approximately 20% of all blood products transfused are associated with coronary artery bypass grafting procedures. Transfusion of allogenic blood products is associated with well-documented morbidity and increased mortality after cardiac surgery. Enhanced fibrinolysis contributes to increased blood product transfusion in the perioperative period. The current proposal tests the central hypothesis that endogenous bradykinin contributes to the hemodynamic, fibrinolytic and inflammatory response to CPB and that bradykinin receptor antagonism will reduce hypotension, inflammation and transfusion requirements. In SPECIFIC AIM 1 we will test the hypothesis that the fibrinolytic and inflammatory response to CPB differ during ACE inhibition and angiotensin II type 1 receptor antagonism. In SPECIFIC AIM 2 we will test the hypothesis that bradykinin B2 receptor antagonism attenuates the hemodynamic, fibrinolytic, and inflammatory response to CPB. In SPECIFIC AIM 3 we will test the hypothesis that bradykinin B2 receptor antagonism reduces the risk of allogenic blood product transfusion in patients undergoing CPB. These studies promise to provide important information regarding the effects of drugs that interrupt the RAS and generate new strategies to reduce morbidity in patients undergoing CPB.
NCT00223704 ↗	Bradykinin Receptor Antagonism During Cardiopulmonary Bypass	Completed	Vanderbilt University Medical Center	Phase 2/Phase 3	2006-05-01	Each year over a million patients worldwide undergo cardiac surgery requiring cardiopulmonary bypass (CPB). CPB is associated with significant morbidity including the transfusion of allogenic blood products, inflammation and hemodynamic instability. In fact, approximately 20% of all blood products transfused are associated with coronary artery bypass grafting procedures. Transfusion of allogenic blood products is associated with well-documented morbidity and increased mortality after cardiac surgery. Enhanced fibrinolysis contributes to increased blood product transfusion in the perioperative period. The current proposal tests the central hypothesis that endogenous bradykinin contributes to the hemodynamic, fibrinolytic and inflammatory response to CPB and that bradykinin receptor antagonism will reduce hypotension, inflammation and transfusion requirements. In SPECIFIC AIM 1 we will test the hypothesis that the fibrinolytic and inflammatory response to CPB differ during ACE inhibition and angiotensin II type 1 receptor antagonism. In SPECIFIC AIM 2 we will test the hypothesis that bradykinin B2 receptor antagonism attenuates the hemodynamic, fibrinolytic, and inflammatory response to CPB. In SPECIFIC AIM 3 we will test the hypothesis that bradykinin B2 receptor antagonism reduces the risk of allogenic blood product transfusion in patients undergoing CPB. These studies promise to provide important information regarding the effects of drugs that interrupt the RAS and generate new strategies to reduce morbidity in patients undergoing CPB.
NCT00320619 ↗	Epsilon-Aminocaproaic Acid to Reduce the Need for Blood Transfusions During and Following Spine Surgery	Completed	National Heart, Lung, and Blood Institute (NHLBI)	N/A	2000-09-01	Individuals who undergo spine surgery often have a significant loss of blood and may require multiple blood transfusions. Research has shown that epsilon-aminocaproic acid (EACA) may reduce the amount of blood lost during surgery, which would decrease the number of blood transfusions required. This study will evaluate the safety and effectiveness of EACA at reducing blood loss and the need for blood transfusions in individuals undergoing spine surgery.

Clinical Trial Conditions for aminocaproic acid

Condition Name

Condition Name for aminocaproic acid
Intervention	Trials
Blood Loss, Surgical	4
Bleeding	3
Blood Loss	3
Craniosynostosis	2

Condition MeSH

Condition MeSH for aminocaproic acid
Intervention	Trials
Hemorrhage	16
Blood Loss, Surgical	4
Osteoarthritis	3
Inflammation	2

Clinical Trial Locations for aminocaproic acid

Trials by Country

Trials by Country for aminocaproic acid
Location	Trials
United States	41
Egypt	6
Canada	2
Brazil	2
Mexico	2

Trials by US State

Trials by US State for aminocaproic acid
Location	Trials
New York	5
Illinois	3
Georgia	3
North Carolina	3
California	3

Clinical Trial Progress for aminocaproic acid

Clinical Trial Phase

Clinical Trial Phase for aminocaproic acid
Clinical Trial Phase	Trials
PHASE4	1
Phase 4	12
Phase 3	3

Clinical Trial Status

Clinical Trial Status for aminocaproic acid
Clinical Trial Phase	Trials
Completed	27
Unknown status	4
Recruiting	3

Clinical Trial Sponsors for aminocaproic acid

Sponsor Name

Sponsor Name for aminocaproic acid
Sponsor	Trials
Duke University	2
Texas Children's Hospital	2
Emory University	2

Sponsor Type

Sponsor Type for aminocaproic acid
Sponsor	Trials
Other	52
Industry	2
NIH	2

Aminocaproic Acid: Clinical Trials Update and Market Outlook

Last updated: April 28, 2026

Aminocaproic acid (ACA) is an established hemostatic agent used to reduce bleeding by inhibiting fibrinolysis. Clinical activity in 2024 to 2026 is largely incremental and indication-specific, centered on bleeding management in settings such as surgery, trauma, and obstetrics, with trial designs that typically compare ACA to placebo or alternative antifibrinolytics (or evaluate dosing strategies). Market demand is supported by continued perioperative use and the drug’s long-established availability, while pricing and volume growth are constrained by generic competition and mature prescribing patterns.

What clinical trials are active or recently reported for aminocaproic acid?

Trial landscape (where activity is concentrated)

Across public registries and sponsor reporting patterns, aminocaproic acid trial updates cluster into three practical buckets:

1. Perioperative bleeding and antifibrinolytic optimization

   • Focus: dosing regimens, route (oral vs intravenous), and patient selection.
   • Typical comparator logic: placebo or another antifibrinolytic (often tranexamic acid in contemporary protocols).
   • Common endpoints: measured blood loss, transfusion requirement, and clinically relevant bleeding scores.

2. Trauma bleeding and early hemostasis windows

   • Focus: early administration timing, target population (major trauma, high bleeding risk), and safety outcomes.
   • Endpoints: mortality, transfusion, thromboembolic events, and bleeding volume.

3. Obstetric hemorrhage (postpartum bleeding) and uterine bleeding

   • Focus: prevention or treatment of postpartum hemorrhage and reduction in escalation to additional hemostatic interventions.
   • Endpoints: blood loss metrics, need for uterotonics/surgery, and adverse events.

What the “update” looks like in market-relevant terms

For an established, off-patent molecule, the trial cycle is less about first-in-class efficacy proof and more about:

• Label-adjacent optimization (dose, route, timing, and subpopulations)
• Comparative positioning against modern antifibrinolytics, especially tranexamic acid
• Safety reaffirmation in contemporary care pathways, particularly thrombosis-risk characterization

Evidence quality for decision-making

In mature antifibrinolytic classes, regulators and clinicians tend to weigh:

• Consistency of effect on bleeding and transfusion outcomes
• The size of clinically meaningful endpoints (not only laboratory measures)
• Thromboembolic and renal safety signals under current standard-of-care

For ACA specifically, the practical implication is that trials that show a credible reduction in transfusion or escalation of hemorrhage therapy can translate into adoption, while small mechanistic or surrogate-only studies usually have limited market impact.

How does the current evidence base translate into prescribing and guideline behavior?

Mechanism and clinical role

Aminocaproic acid inhibits fibrinolysis by blocking lysine binding sites on plasminogen, reducing conversion to plasmin and stabilizing clots. Clinicians use it when excessive fibrinolysis drives bleeding, particularly in:

• Surgical fields with high bleeding risk
• Settings where transfusion exposure is to be minimized
• Acute hemorrhage scenarios where early hemostasis matters

Adoption drivers

Market adoption tracks to four practical levers:

• Clinical pathways: hospital protocols for perioperative blood conservation and trauma/obstetric hemorrhage
• Formulary availability: generic pricing and supply continuity
• Comparative preference: where tranexamic acid has stronger adoption, ACA trials need clear differentiation or niche advantages
• Operational ease: dosing simplicity and route compatibility with existing emergency and perioperative workflows

What is the market size and demand profile for aminocaproic acid?

Market structure

Aminocaproic acid is widely genericized in many jurisdictions, which typically creates:

• Competitive pricing pressure
• High volume but limited price growth
• Fragmented supplier landscape
• Demand dominated by routine clinical use rather than breakthrough uptake

Demand segmentation (where volume is generated)

Forecastable demand concentrates in:

• Hospitals and ambulatory surgery centers that stock antifibrinolytics
• Emergency and trauma centers for acute bleeding workflows
• Women’s health units for obstetric hemorrhage readiness
• Specialty centers that use ACA for specific bleeding conditions or protocols

Competitive context

In antifibrinolysis, the competitive “shadow price” is usually set by tranexamic acid. That affects ACA’s market outcome via:

• Formulary switching when TXA is preferred
• Trial-driven re-optimization when ACA is shown to be noninferior or superior on transfusion/bleeding endpoints in a niche

What market projections should investors and R&D leaders model for aminocaproic acid?

Baseline projection logic (mature, generic market)

For an off-patent molecule:

• Volume growth tends to track hospital procedure volume and protocol intensity (perioperative and acute hemorrhage programs).
• Revenue growth is constrained by generic price elasticity and purchasing consolidation.

A realistic projection model for ACA typically assumes:

• Low to moderate volume growth
• Limited to modest revenue growth unless there is meaningful uptake in a large protocol segment or a supply-driven pricing change

Scenario framework (projectable drivers)

Market upside tends to come from:

• New evidence that supports guideline expansion in a high-volume indication segment (trauma or obstetrics)
• Protocol adoption that embeds ACA as a standard option
• Formulation or route changes that reduce administration friction (where that changes real-world uptake)

Market downside is driven by:

• Switching to tranexamic acid in protocols that allow interchangeability
• Cost-based formulary pressure that consolidates purchasing to the lowest net cost antifibrinolytic
• Supply interruptions in the generic supply chain that reduce throughput temporarily (more a volatility factor than structural growth)

How does the pipeline look for future clinical differentiation?

Where differentiation is most likely

The highest probability differentiation areas for ACA in a post-generic, post-label-maturity environment are:

• Narrow indication niches where fibrinolysis biology and timing create a measurable advantage
• Dosing strategy that improves efficacy-to-safety ratio under contemporary standards
• Combination protocols (e.g., with transfusion management bundles) where ACA’s effect is measurable in real-world endpoints

What trial designs matter for adoption

Trials that support uptake tend to:

• Use clinically meaningful endpoints such as transfusion rates, bleeding volume, and escalation to invasive hemostasis
• Include robust safety monitoring for thrombosis signals
• Reflect current care pathways so results are reproducible in practice

What should a market entry or development plan assume about IP and commercial timing?

IP reality for aminocaproic acid

ACA is not an IP-led molecule in the way new drug candidates are; the practical commercial question is not “who owns the molecule,” but:

• which company controls supply and formulation,
• who has the best distribution footprint,
• who can attach new clinical differentiation to gain formulary share.

Commercial timing

Because ACA is mature, time-to-impact depends on:

• Trial-to-guideline translation cycles
• Pharmacy and therapeutics committee adoption windows
• Procurement cycles and tender timing
• Implementation of protocol changes across hospital networks

Key takeaways for clinical strategy and investment thesis

• Aminocaproic acid is a mature, generic antifibrinolytic with clinical use concentrated in perioperative bleeding, trauma, and obstetric hemorrhage pathways.
• Recent trial activity is likely indication and protocol specific, focused on bleeding endpoints and transfusion reduction, with comparative positioning versus tranexamic acid in modern antifibrinolytic algorithms.
• Market growth expectations should reflect generic price compression and stable demand from hospital stock and emergency readiness, with upside only if new evidence expands protocol usage in a high-volume segment or improves real-world adoption.
• The development strategy that creates market traction for ACA is evidence generation tied to clinically meaningful endpoints and care pathway fit, not surrogate endpoints alone.

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Key Takeaways

• Clinical activity focuses on indication-specific hemorrhage management and dosing optimization rather than first-in-class proof.
• Adoption depends on transfusion and clinically relevant bleeding outcomes plus safety reproducibility under current standards.
• Market outlook is constrained by generics; revenue growth is sensitive to protocol share and purchasing economics more than pricing power.
• Best-case upside comes from trials that change guideline or protocol behavior in large-volume settings like trauma or postpartum hemorrhage.

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FAQs

1) Is aminocaproic acid still used clinically at scale?

Yes. ACA remains a standard antifibrinolytic option in multiple hospital protocols, especially where perioperative and acute hemorrhage management protocols embed lysine-analog antifibrinolysis.

2) How does aminocaproic acid compete against tranexamic acid?

The main competitive lever is formulary preference shaped by trial evidence, clinician familiarity, and net cost. ACA must show clear clinical or workflow advantages in specific niches to gain share.

3) What trial endpoints most influence prescribing for aminocaproic acid?

Transfusion requirements, clinically relevant bleeding measures, escalation to additional hemostatic interventions, and thromboembolic safety outcomes are the most adoption-relevant endpoints.

4) What drives market growth for a mature generic like aminocaproic acid?

Market growth is driven by volume expansion through protocol inclusion and hospital network uptake, while revenue growth is constrained by price competition and consolidated procurement.

5) What is the most plausible path to commercial differentiation for aminocaproic acid?

Indication and protocol differentiation supported by clinically meaningful trial results, aligned with contemporary care pathways and measurable improvements in bleeding and transfusion outcomes.

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References

[1] ClinicalTrials.gov. Aminocaproic acid (search results and trial listings). U.S. National Library of Medicine.
[2] European Medicines Agency (EMA). Product information and assessment materials for aminocaproic acid (where applicable).
[3] U.S. FDA. Drug label and approved uses for aminocaproic acid (where applicable).