Comparing High and lOw-dose asPirin With Dual anTIplatelet Therapy for Three Months Using prasUgrel and aSpirin Following Coronary Artery Bypass Grafting. (OPTIMUS-CABG Trial)

The purpose of this study is to compare the effect of prasugrel plus low-dose aspirin versus high dose aspirin alone (300mg) and versus low dose aspirin alone (75 mg) in patients with chronic coronary disease undergoing coronary artery bypass grafting.

Start Date31 Oct 2025

Sponsor / Collaborator

Medical Research Agency

NCT07025148

/ RecruitingPhase 4IIT

Switching From Clopidogrel to Low-dose Prasugrel in Patients at Dual-risk Following Percutaneous Coronary Intervention (TAILOR-BLEED-2)

The primary aim of this study is to investigate the PD effects of switching from standard-dose clopidogrel dose to low-dose prasugrel versus continuing standard-dose clopidogrel in patients at dual-risk (HBR defined as the HBR-ARC criteria and HIR defined as ABCD-GENE score ≥10) following PCI. We hypothesize that in patients at dual-risk, switching from standard-dose clopidogrel to low-dose prasugrel will be superior to continuing standard-dose clopidogrel in terms of platelet reactivity.

Start Date01 Oct 2025

Sponsor / Collaborator

University of Florida

NCT06916520

/ Not yet recruitingPhase 4IIT

Prasugrel Monotherapy Reduced Dose in Acute and Chronic Coronary Syndrome Patients After Percutaneous Coronary Intervention

Rationale: Dual antiplatelet therapy, consisting of aspirin and a P2Y12-inhibitor, reduces the risk of stent-related and non-stent-related ischemic events after percutaneous coronary intervention (PCI). However, this therapy is also associated with a higher risk of bleeding. Given the advances in stent technology and pharmacology, it may be possible to treat patients undergoing PCI with low dose prasugrel as single antiplatelet therapy, regardless of medical history, age or body weight.
Objective: Assess the feasibility and safety of a single antiplatelet strategy with a reduced dose of prasugrel 5 mg after PCI in acute and chronic coronary syndrome patients (ACS and CCS).
Study design: Open-label, single-centre, randomized controlled trial pilot.
Study population: Patients undergoing successful PCI due to acute or chronic coronary syndrome.
Intervention: A once-daily reduced dose of 5 mg prasugrel for 6 months in CCS patients and for 12 months in ACS patients, preceded by a loading dose of 60 mg prasugrel after PCI, administered without concomitant use of aspirin.
Main study parameters/endpoints: The primary endpoint is Net Adverse Clinical Events (NACE), a composite of all-cause death, myocardial infarction, definite stent thrombosis, ischemic stroke, clinically relevant non-major bleeding or major bleeding defined as Bleeding Academic Research Consortium type 2, 3 or 5.

Start Date01 Sep 2025

Sponsor / Collaborator-

100 Clinical Results associated with Prasugrel Hydrochloride

100 Translational Medicine associated with Prasugrel Hydrochloride

100 Patents (Medical) associated with Prasugrel Hydrochloride

3,190

Literatures (Medical) associated with Prasugrel Hydrochloride

01 Jan 2026·INTERNATIONAL JOURNAL OF CARDIOLOGY

Ticagrelor/Prasugrel or clopidogrel in acute coronary syndrome and advanced chronic kidney disease: Is more potency worth the risk?

Author: Pan, Deng ; Guo, Xinru

31 Dec 2025·PLATELETS

Pharmacodynamic effects of early aspirin withdrawal after percutaneous coronary intervention in patients with atrial fibrillation treated with ticagrelor or prasugrel

Article

Author: Bridge, Claire ; Hanson, Jessica ; Maz, Emily ; Judge, Heather ; Williamson, Georgia ; Middle, Janet ; Storey, Robert F ; Sammut, Mark A ; Lynch, Bethany ; Rahman, Mohammed E F ; McMellon, Hannah ; Lee, Justin ; Parker, William A E

Dual antithrombotic therapy (DAT) without aspirin reduces bleeding compared with triple antithrombotic therapy (TAT) in patients with atrial fibrillation who have undergone percutaneous coronary intervention, without apparently increasing ischemic events. A prospective pharmacodynamic study was performed to investigate the impact of aspirin on bleeding time, platelet function and fibrin clot analysis in this population. Patients receiving TAT (n = 16), comprising aspirin, ticagrelor/prasugrel and a direct-acting oral anticoagulant (DOAC), were compared with those receiving DAT without aspirin (n = 18). Bleeding time was reduced with DAT compared with TAT (median 27.8 vs 30.0 minutes, p = .005). Assessed by light transmission aggregometry, median platelet aggregation was significantly increased with DAT compared with TAT in response to arachidonic acid (63 vs 3%, p = .002) and collagen (72 vs 37%, p < .001) but not 5-μmol/L adenosine diphosphate (25 vs 27%, p = .966) or thrombin-receptor-activating peptide (37 vs 24%, p = .086). VerifyNow P2Y₁₂ assay showed > 70% inhibition in all patients. Fibrin clot lysis time and maximum turbidity were similar between groups. Using P2Y₁₂ inhibitors of consistent potency, DAT improves hemostasis through sparing cyclooxygenase-1-mediated platelet activation but has a comparable effect to TAT on other pathways and fibrin clot properties. DAT with ticagrelor/prasugrel and DOAC may provide sufficient antithrombotic effect without excessive anti-hemostatic effect.

01 Dec 2025·BIOCHEMICAL PHARMACOLOGY

Promising clopidogrel analogs may overcome clopidogrel resistance: 2025 update

Review

Author: Jia, Yu-Meng ; Mi, Qiong-Yu ; Ji, Jin-Zi ; Jiang, Li-Ping ; Tai, Ting ; Xie, Hong-Guang

Clopidogrel is one of the World Health Organization-recommended essential medicines used for antiplatelet therapy. However, its usage is limited by resistance of certain patients to clopidogrel. Herein, we systematically summarized promising novel analogs of clopidogrel and evaluated their preclinical and clinical properties as well as the science behind the study. The primary strategy of their design and synthesis is largely focused on how to enhance their metabolic activation, significantly increasing the systemic exposure of their active thiol metabolites (such as H4). Of these, DT-678 released H4 into the blood following exposure to GSH due to bypassing all cytochrome P450-mediated metabolic activation processes of clopidogrel; evategrel (formerly CG-0255) was converted to H4 by esterase-catalyzed hydrolysis. Vicagrel, acetate of clopidogrel, was completely hydrolyzed to 2-oxo-clopidogrel by intestinal hydrolases, thus bypassing the first-step oxidation of clopidogrel and consequently increasing the formation of H4. The same strategies as those for prasugrel and vicagrel were used to design new compounds, such as tipidogrel, compound 6b, PLD-301, and W-1. In addition, 2-oxo-clopidogrel, an intermediate metabolite shared by clopidogrel, vicagrel, PLD-301, and W-1, was used to determine whether it could exert the same antiplatelet effect as its parent drugs. Moreover, clopidogrel and vicagrel were also deuterated to further increase the formation of H4 in the liver. All these new compounds in the pipeline are promising antiplatelet drugs, and superior to clopidogrel. DT-678 and evategrel are considered the best clopidogrel analogs that may overcome clopidogrel resistance due to their superior efficacy and safety profiles over clopidogrel.

News (Medical) associated with Prasugrel Hydrochloride

17 Dec 2024

·www.accesswire.com

Esteemed Harvard Medical School Professor Dr. Michael Gibson Appointed Chief Medical Advisor at Lexaria Bioscience

Dr. Gibson joining Lexaria's new scientific advisor board KELOWNA, BC / ACCESSWIRE / December 17, 2024 / Lexaria Bioscience Corp. (NASDAQ:LEXX)(NASDAQ:LEXXW) (the "Company" or "Lexaria"), a global innovator in drug delivery platforms, announces the appointment of Dr. Michael Gibson as its new Chief Medical Advisor. Dr. Gibson will collaborate directly with President John Docherty as Lexaria's patented DehydraTECH drug delivery platform continues to expand its applications in GLP-1 and hypertension.C. Michael Gibson M.S., M.D., is an interventional cardiologist, cardiovascular researcher & educator. He is the CEO of the combined non-profit Baim and PERFUSE research institutes at Harvard Medical School. Gibson founded PERFUSE in 1987 which served as the TIMI Data coordinating center that coordinated data for the first 50 TIMI trials. The Baim institute was formerly known as Harvard Clinical Research Institute and was founded in 2000.The combined institutes have led over 1,250 studies, published 5,500 manuscripts in peer review literature (including 144 in the New England Journal of Medicine) and have led 70 FDA submissions from their network of 7,000 sites in 57 countries worldwide. Since 2014, Gibson has consistently been ranked as one of the world's most highly cited authors in all of science by Thomson Reuters. In 2021, he was named one of the Fifty of the Most Influential Voices in Healthcare by Medika Life. His work has been cited over 170,000 times."Lexaria's drug delivery technology offers exciting new pathways towards improving pharmacokinetic drug performance that could unlock a new era of reduced drug waste and adverse side effects combined with enhanced efficacy," said Dr. Gibson. "I'm excited to pursue new and improved applications for this exciting technology.""Dr. Gibson has a wealth of knowledge and experience that will benefit Lexaria, particularly in the area of hypertension which remains an area of intense interest for Lexaria," said John Docherty, President. "On behalf of everyone at Lexaria, I welcome Dr. Gibson's contributions as our new Chief Medial Advisor and member of our scientific advisory board."As Chief Medical Advisor, Dr. Gibson will participate with other scientific and medical experts within Lexaria's newly-formed scientific advisory board in pursuing Lexaria's prioritized objectives in the fields of drug delivery optimization.Dr. Gibson has led phase 1-4 clinical trials, and cardiology megatrials of over 34,000 patients which eventuate in international approval of drugs like prasugrel, rivaroxaban, betrixaban and andexanet as well as devices such as one that alarms to alert a patient to heart attack. He founded WikiDoc.org and WikiPatient.org and is Editor-In-Chief of over 2,200 active contributors who have edited the content of over 100,000 chapters millions of times over the past 15 years. Gibson also founded www.clinicaltrialresults.org. Gibson serves as Chief Medical Correspondent for the American College of Cardiology. Gibson has over 435,000 followers on social media where he is a leading influencer, second only to Sanjay Gupta in some pollsAbout Lexaria Bioscience Corp. & DehydraTECHDehydraTECH™ is Lexaria's patented drug delivery formulation and processing platform technology which improves the way active pharmaceutical ingredients (APIs) enter the bloodstream through oral delivery. Since 2016, Lexaria has developed and investigated DehydraTECH with a variety of beneficial molecules in oral and topical formats. DehydraTECH has repeatedly demonstrated the ability to increase bio-absorption and has also evidenced an ability to deliver some drugs more effectively across the blood brain barrier, which Lexaria believes to be of particular importance for centrally active compounds. Lexaria operates a licensed in-house research laboratory and holds a robust intellectual property portfolio with 46 patents granted and many patents pending worldwide. For more information, please visit www.lexariabioscience.com.CAUTION REGARDING FORWARD-LOOKING STATEMENTSThis press release includes forward-looking statements. Statements as such term is defined under applicable securities laws. These statements may be identified by words such as "anticipate," "if," "believe," "plan," "estimate," "expect," "intend," "may," "could," "should," "will," and other similar expressions. Such forward-looking statements in this press release include, but are not limited to, statements by the company relating the Company's ability to carry out research initiatives, receive regulatory approvals or grants or experience positive effects or results from any research or study. Such forward-looking statements are estimates reflecting the Company's best judgment based upon current information and involve a number of risks and uncertainties, and there can be no assurance that the Company will actually achieve the plans, intentions, or expectations disclosed in these forward-looking statements. As such, you should not place undue reliance on these forward-looking statements. Factors which could cause actual results to differ materially from those estimated by the Company include, but are not limited to, government regulation and regulatory approvals, managing and maintaining growth, the effect of adverse publicity, litigation, competition, scientific discovery, the patent application and approval process, potential adverse effects arising from the testing or use of products utilizing the DehydraTECH technology, the Company's ability to maintain existing collaborations and realize the benefits thereof, delays or cancellations of planned R&D that could occur related to pandemics or for other reasons, and other factors which may be identified from time to time in the Company's public announcements and periodic filings with the US Securities and Exchange Commission on EDGAR. The Company provides links to third-party websites only as a courtesy to readers and disclaims any responsibility for the thoroughness, accuracy or timeliness of information at third-party websites. There is no assurance that any of Lexaria's postulated uses, benefits, or advantages for the patented and patent-pending technology will in fact be realized in any manner or in any part. No statement herein has been evaluated by the Food and Drug Administration (FDA). Lexaria-associated products are not intended to diagnose, treat, cure or prevent any disease. Any forward-looking statements contained in this release speak only as of the date hereof, and the Company expressly disclaims any obligation to update any forward-looking statements or links to third-party websites contained herein, whether as a result of any new information, future events, changed circumstances or otherwise, except as otherwise required by law.INVESTOR CONTACT:George Jurcic - Head of Investor Relations[email protected]Phone: 250-765-6424, ext 202SOURCE: Lexaria Bioscience Corp.

Executive Change

24 Nov 2023

·synapse.patsnap.com

What are COX inhibitors and how do you quickly get the latest development progress?

COX, or cyclooxygenase, is an enzyme that plays a crucial role in the human body's inflammatory response. It is responsible for the production of prostaglandins, which are hormone-like substances involved in various physiological processes. COX exists in two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed and involved in maintaining normal bodily functions, such as protecting the stomach lining and regulating blood clotting. On the other hand, COX-2 is induced during inflammation and is primarily responsible for the production of prostaglandins that cause pain, fever, and swelling. Understanding the role of COX has led to the development of drugs called COX inhibitors, which are used to manage pain, inflammation, and other related conditions. COX inhibitors, can be categorized into two main types. The first are non-selective COX inhibitors, which can simultaneously inhibit both COX-1 and COX-2 enzymes, with Aspirin being a primary example. The second type involves selective COX-2 inhibitors, such as celecoxib, which was the first COX-2-specific inhibitor approved by the FDA for use in the treatment of familial adenomatous polyposis (FAP). There are two isozymes of cyclooxygenase, namely COX-1 and COX-2. COX-1 is an always-present enzyme in different tissues, including the stomach lining, platelets, and kidneys. On the other hand, COX-2 is an enzyme generally induced in the context of inflammation or tissue healing. Extensive research indicates that most tumors overexpress COX-2, while the expression of COX-1 shows no significant discrepancies between tumorous and normal tissues. Therefore, studies focusing on the role of cyclooxygenase in tumor progression primarily concern COX-2. The analysis of the target COX reveals a competitive landscape with several companies making progress in the development of COX inhibitors. GSK Plc, Viatris Inc., and Pfizer Inc. are among the companies growing fastest in this area. Pain, rheumatoid arthritis, and osteoarthritis are the most common indications for approved drugs. Small molecule drugs are progressing rapidly, indicating intense competition in the development of innovative drugs. China, the United States, and Japan are the leading countries/locations in COX inhibitors development. Overall, the target COX presents opportunities for further research and development, particularly in addressing pain management and rheumatic conditions. The mechanism of action of COX inhibitorsCOX inhibitors are a type of medication that inhibit the activity of cyclooxygenase (COX) enzymes. These enzymes play a crucial role in the production of prostaglandins, which are chemical messengers involved in inflammation, pain, and fever. COX inhibitors work by blocking the action of COX enzymes, thereby reducing the production of prostaglandins. From a biomedical perspective, COX inhibitors are commonly used in the treatment of pain, inflammation, and fever. They are widely prescribed for conditions such as arthritis, menstrual cramps, headaches, and post-operative pain. By reducing the production of prostaglandins, COX inhibitors help alleviate symptoms associated with these conditions. There are two main types of COX inhibitors: COX-1 inhibitors and COX-2 inhibitors. COX-1 inhibitors, such as aspirin, naproxen, and ibuprofen, inhibit both COX-1 and COX-2 enzymes. They are effective in relieving pain and inflammation but can also cause side effects such as stomach ulcers and bleeding. On the other hand, COX-2 inhibitors, such as celecoxib, selectively inhibit the COX-2 enzyme while sparing COX-1. This selective inhibition reduces the risk of stomach ulcers and bleeding associated with COX-1 inhibitors. COX-2 inhibitors are commonly used for long-term management of chronic conditions like osteoarthritis and rheumatoid arthritis. In summary, COX inhibitors are a class of medications that inhibit the activity of COX enzymes, reducing the production of prostaglandins. They are commonly used to treat pain, inflammation, and fever, with different types of COX inhibitors offering varying degrees of selectivity and side effects. List of COX InhibitorsThe currently marketed COX inhibitors include: Celecoxib/Tramadol HydrochlorideDiclofenac etalhyaluronateBupivacaine/MeloxicamAspirin/Vonoprazan FumarateBirch bark extractPrasugrel Hydrochloride/AspirinDiclofenac/LidocaineEsflurbiprofenAspirin ZincPolmacoxibFor more information, please click on the image below. What is the purpose of using COX inhibitors?COX inhibitors are commonly used for conditions such as angina, atrial fibrillation, arrhythmia, and myocardial infarction.For more information, please click on the image below to log in and search. How to obtain the latest development progress of COX inhibitors?In the Synapse database, you can keep abreast of the latest research and development advances of COX inhibitors anywhere and anytime, daily or weekly, through the "Set Alert" function. Click on the image below to embark on a brand new journey of drug discovery!

15 Nov 2021

·endpts.com

Eyeing an accelerated BLA, PhaseBio says its monoclonal antibody reversed the dangerous effects of AstraZeneca's blood thinner

A class of blood thinners called P2Y12 inhibitors has been used for the last couple decades to treat and prevent a range of cardiovascular conditions, including stroke and heart attack. But the antiplatelet drugs come with a risk of increased bleeding, which can prove fatal — especially for those who need urgent surgery and don’t have time to wean off their medication. PhaseBio is working on a solution for that. And on Monday, the company presented positive Phase III data that could pave the way for a mid-2022 BLA submission. The company’s lead drug bentracimab was shown to reverse the effects of AstraZeneca’s blood thinner Brilinta in an interim analysis of more than 100 patients who needed urgent surgery or an invasive procedure, PhaseBio announced at this year’s American Heart Association conference. Patients who took bentracimab in the pivotal REVERSE-IT trial saw a 135% reduction in platelet inhibition within 5 to 10 minutes of infusion (p<0.001) and saw those effects last over 24 hours, according to PhaseBio. The drug also met its co-primary endpoint, defined as good or excellent hemostasis within 24 hours of administration. Regulators previously told PhaseBio that an interim analysis from the first 100 patients in REVERSE-IT would be sufficient for an accelerated BLA submission, CEO Jonathan Mow told Endpoints News. “When we then looked at the Phase III data and saw that not only did we hit the VerifyNow, platelet biomarker endpoint, we also hit the clinical endpoint — albeit with a slightly larger number of patients, you know, 150 in total — but still, that’s a fantastic achievement for us. One that was not expected at this point in time,” he said. Bentracimab appeared safe, according to PhaseBio. And though 91% of patients reported a treatment-emergent side effect, the most common was pain associated with the surgical procedure. Eight experienced thrombotic events, though none of the cases were tied to bentracimab. “With no approved reversal agents for oral P2Y12 inhibitors, patients who are prescribed these medications to reduce the risk of cardiac events are at increased risk for spontaneous major bleeding events, and physicians are faced with a complex dilemma of balancing bleeding risk and thrombotic risk, should these patients require urgent surgery,” said Deepak Bhatt, executive director of interventional cardiovascular programs at Boston’s Brigham and Women’s Hospital, who presented the study at AHA. Doctors typically recommend patients stop taking P2Y12 inhibitors five to seven days before any type of surgical procedure. But while other P2Y12 inhibitors like Sanofi’s Plavix and Eli Lilly’s Effient aren’t reversible, Brilinta is. That’s because Plavix and Effient bind to the P2Y12 receptor permanently, so to regain functionality, you need to wait for platelet turnover. Brilinta, on the other hand, binds transiently and only has about a 15-minute residence time on the receptor. Bentracimab is a monoclonal antibody fragment that binds to Brilinta when it’s in that off state, and removes it from the platelet environment. “Essentially it just sequesters ticagrelor [Brilinta] from the platelet,” CMO John Lee told Endpoints. The Phase III readout comes just a couple weeks after PhaseBio reported positive topline results for a Phase IIb study evaluating bentracimab in healthy, older volunteers on Brilinta. Earlier results have also shown promise in treating younger volunteers. The news also bodes well for the Italian biotech Alfasigma, which back in June put down up to $245 million for the European rights to bentracimab. PhaseBio originally licensed the drug from MedImmune, the biologics arm of AstraZeneca, in 2017 for an upfront fee of $100,000, with $68 million in potential milestones. A little over a year later, the biotech rode that deal to an IPO with MedImmune owning 5% of the stock. And in 2019, bentracimab received breakthrough therapy designation from the FDA. While bentracimab would be the first antiplatelet reversal therapy for a P2Y12 inhibitor, it would not be the first to address the risk of bleeding in patients on blood thinners. Back in 2018, the FDA approved Portola Pharmaceuticals’ Andexxa as the first reversal agent for Factor Xa inhibitors, such as Janssen’s Xarelto and Bristol Myers Squibb and Pfizer’s Eliquis. PhaseBio is still recruiting patients with uncontrolled major or life-threatening bleeding for the REVERSE-IT trial, and aims to be fully-enrolled as soon as possible.

AntibodyBreakthrough TherapyAHAIPO

100 Deals associated with Prasugrel Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
D05597	Prasugrel Hydrochloride	B01AC22	DB06209

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Brain Ischemia	Japan	Daiichi Sankyo Co., Ltd.	24 Dec 2021
Angina, Stable	Japan	Daiichi Sankyo Co., Ltd.	24 Mar 2014
Myocardial Infarction	Japan	Daiichi Sankyo Co., Ltd.	24 Mar 2014
Acute Coronary Syndrome	European Union	Vygoris Ltd.	24 Feb 2009
Acute Coronary Syndrome	Iceland	Vygoris Ltd.	24 Feb 2009
Acute Coronary Syndrome	Liechtenstein	Vygoris Ltd.	24 Feb 2009
Acute Coronary Syndrome	Norway	Vygoris Ltd.	24 Feb 2009
Angina, Unstable	European Union	Vygoris Ltd.	24 Feb 2009
Angina, Unstable	Iceland	Vygoris Ltd.	24 Feb 2009
Angina, Unstable	Liechtenstein	Vygoris Ltd.	24 Feb 2009
Angina, Unstable	Norway	Vygoris Ltd.	24 Feb 2009
Non-St Elevated Myocardial Infarction	European Union	Vygoris Ltd.	24 Feb 2009
Non-St Elevated Myocardial Infarction	Iceland	Vygoris Ltd.	24 Feb 2009
Non-St Elevated Myocardial Infarction	Liechtenstein	Vygoris Ltd.	24 Feb 2009
Non-St Elevated Myocardial Infarction	Norway	Vygoris Ltd.	24 Feb 2009
ST Elevation Myocardial Infarction	European Union	Vygoris Ltd.	24 Feb 2009
ST Elevation Myocardial Infarction	Iceland	Vygoris Ltd.	24 Feb 2009
ST Elevation Myocardial Infarction	Liechtenstein	Vygoris Ltd.	24 Feb 2009
ST Elevation Myocardial Infarction	Norway	Vygoris Ltd.	24 Feb 2009

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Anemia, Sickle Cell	Phase 3	United States	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Belgium	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Brazil	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Canada	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Egypt	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Ghana	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Italy	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Kenya	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Lebanon	Eli Lilly & Co.	01 Apr 2013
Anemia, Sickle Cell	Phase 3	Oman	Eli Lilly & Co.	01 Apr 2013

Clinical Result

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Phase

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESC2024	Not Applicable	Non-St Elevated Myocardial Infarction	-	Prasugrel monotherapy (3.75mg/day)	eghpobovqy(vkdjypkyqj) = fiflabhiua rrcqexgpgp (lyrqlwzvod ) View more	-	01 Sep 2024
ESC2024	Not Applicable	Myocardial Infarction	-	Prasugrel	xtabkrjxxa(jjalnhvarp): HR = 0.67 (95% CI, 0.47 - 0.95) View more	-	30 Aug 2024
				Ticagrelor
NCT04668144 (SWAP-6, CTgov)	Phase 4	Acute Coronary Syndrome \| Coronary Artery Disease \| Non ST segment elevation acute coronary syndrome	359	Prasugrel (Prasugrel)	vmhhzvcqyi(lhxibtxdcr) = fwszhrdomk syajbmtkyl (gjfkjffvah, 31) View more	-	20 Mar 2024
				Cangrelor+Prasugrel (Prasugrel + Cangrelor)	vmhhzvcqyi(lhxibtxdcr) = slvgaaxzyz syajbmtkyl (gjfkjffvah, 104) View more
NCT05223335 (CTgov)	Phase 4	Hemorrhage	98	Tricagrelor+Prasugrel (Genotype-Guided Therapy)	wjcrgepyha = stbkzcbrxy iqgjfkgkph (dywvxjkull, kelabskhph - sdwsohgqvz) View more	-	21 Feb 2024
				Clopidogrel (Conventional Therapy)	wjcrgepyha = plwuywxnjy iqgjfkgkph (dywvxjkull, viijwspqpg - ozdrcrnbky) View more
NCT01944800 (ISAR-REACT 5, ESC2023)	Phase 4	Acute Coronary Syndrome	-	Ticagrelor	sigembrvbn(vqgxiostdq): HR = 1.62 (95% CI, 1.09 - 2.41)	Negative	27 Aug 2023
				Prasugrel
NCT01944800 (ISAR-REACT 5, Pubmed \| Arterioscler Thromb Vasc Biol)	Phase 4	Acute Coronary Syndrome immature platelet fraction	-	prasugrel	qdysdhdnyg(yaszpvntci) = dkubcvoect xfroetirvw (mxqbzvonsx, 2.5 - 5.2)	-	01 Feb 2023
				ticagrelor	qdysdhdnyg(yaszpvntci) = uxjvtjftfg xfroetirvw (mxqbzvonsx, 2.5 - 5.4)
NCT02193971 (HOST-REDUCE-POLYTECH-ACS, Pubmed \| Eur Heart J Cardiovasc Pharmacother)	Not Applicable	Acute Coronary Syndrome	-	Prasugrel 5 mg daily	elbskrvsrr(jvwhseslzw): HR = 0.66 (95% CI, 0.43 - 0.99), P-Value = 0.049 View more	Positive	28 Jan 2023
				Prasugrel 10 mg daily
NCT01765400 (CTgov)	Phase 4	Heart Failure, Systolic	30	Prasugrel 10 mg daily x 2 weeks (Prasugrel)	ghluyapwfr(fkwyzonbbm) = nasgskbmjf vnnyacuxzj (ipzbqgrwtx, 51.5) View more	-	30 Nov 2022
				Clopidogrel 75 mg daily x 2 weeks (Clopidogrel)	ghluyapwfr(fkwyzonbbm) = qhwjfdqtyg vnnyacuxzj (ipzbqgrwtx, 51.5) View more
NCT01944800 (ISAR-REACT-5, Pubmed \| Eur Heart J Cardiovasc Pharmacother)	Not Applicable	Acute Coronary Syndrome	-	Prasugrel-based strategy	rtlyeturft(ikkvwplnsm): HR = 0.96 (95% CI, 0.75 - 1.25) View more	-	26 Nov 2022
				Ticagrelor-based strategy
NCT01944800 (ISAR-REACT 5, Pubmed \| Circ Cardiovasc Interv)	Phase 4	Acute Coronary Syndrome	3,239	Ticagrelor	tewtmbzyco(ouejrnqrgo): HR = 1.09 (95% CI, 0.73 - 1.62) View more	Positive	01 Oct 2022
				Prasugrel

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