The goal of this clinical study is to learn if adding a medicine called cilostazol to usual treatment can help prevent another stroke, a heart attack, or death in patients who had a stroke caused by a blocked blood vessel, or a "mini-stroke" (also called a TIA), in the past 6 months.
To determine if cilostazol is safe and effective at lowering the chance of strokes, heart attacks and deaths, the study will compare cilostazol to a placebo, a pill that looks the same as cilostazol but has no medicine in it.
Participants will:
* Be assigned by chance to take either cilostazol or a placebo, along with their usual medicine.
* Not know which one they are taking, and neither will the study team, which keeps the results fair.
* Be followed for up to 5 years to see if they have a stroke, heart attack, or major bleeding.

Start Date01 Oct 2026

Sponsor / Collaborator

Stanford University

[+3]

JPRN-jRCTs061260059

/ RecruitingPhase 2

Single-arm exploratory study of cilostazol intervention for glymphatic system dysfunction after subarachnoid hemorrhage.

Start Date27 Aug 2026

Sponsor / Collaborator-

NCT06919835

/ Not yet recruitingPhase 3IIT

CiLostAzol for pReventIon of Recurrent sTroke in Africa

Global estimates suggest that sub-Saharan Africa (SSA) now has the highest incidence, prevalence, and worst survival outcomes of stroke. With an estimated 1.4 million stroke survivors, outcomes of stroke in SSA are abysmal with 1-month case fatality at 30% and 3-year mortality rate of 84%. Stroke survivors in Africa are at an inordinately high (and worsening) risk of adverse outcomes including recurrent stroke and cardiac events over the medium- to longterm. Given the paucity of resources in the region, testing of therapies, which are potentially highly clinically efficacious and cost-effective, while developing local stroke research capacity and contributing to the global secondary stroke prevention evidence base, is urgently needed. Cilostazol, a phosphodiesterase 3 inhibitor, has shown promising efficacy and safety mainly among an Asian population by cutting risk of major adverse cardiovascular events including stroke, in half, when added to aspirin or clopidogrel (8% vs. 4%, HR 0.52, 95% CI 0.35-0.77), with no increased risk in bleeding or serious adverse events. Cilostazol's potentially strong efficacy, presumed pleiotropic effects, and relatively low cost, make it a highly appealing agent for use in stroke-prone, low-resource settings. Therefore, the overall objective of the CiLostAzol for pReventIon of recurrent sTroke in Africa (CLARITY-AFRICA) study is to deploy a hybrid study design to demonstrate the efficacy and safety of cilostazol twice daily in reducing MACE over 24 months vs. placebo among 1100 recent stroke patients encountered at 12 hospitals in Ghana. Secondly, CLARITY-AFRICA also seeks to develop an implementation strategy for routine integration and policy adoption of cilostazol for post-stroke cardiovascular risk reduction in an under-resourced system. Given its compelling efficacy among a predominantly Asian population, the National Institute of Neurological Disorders and Stroke (NINDS) is poised to fund a US-based clinical trial to assess the longer-term efficacy and safety of cilostazol in a study titled CiLostAzol for pReventIon of recurrent sTroke (CLARITY). The investigators are also aware that European and Australian funding agencies are considering stroke trials of cilostazol. A concurrently executed CLARITYAfrica trial would allow recruitment of a historically underrepresented and high-risk group (Africans), test a therapy that if efficacious could be affordable for broader regional implementation, permit transcontinental mentorship/collaborations, and leverage NINDS impending investment. CLARITY-AFRICA will assess implementation outcomes such as adoption, acceptability, cost, pertinent to uptake of cilostazol in Ghana to inform policy. Regardless of its outcome, findings from CLARITYAFRICA will contribute meaningful information from the African perspective to inform the formulation of guidelines for global adoption of cilostazol into routine care for secondary CVD risk prevention by international bodies such as the World Health Organization. This application will focus on the first 2 aims of CLARITY-AFRICA to conduct the trial and assess secondary outcomes.

Start Date01 Aug 2026

Sponsor / Collaborator

Northern California Institute for Research & Education

100 Clinical Results associated with Cilostazol

100 Translational Medicine associated with Cilostazol

100 Patents (Medical) associated with Cilostazol

2,200

Literatures (Medical) associated with Cilostazol

01 Dec 2026·VASCULAR PHARMACOLOGY

The potential of targeting adenosine 5′-monophosphate-activated protein kinase to treat peripheral artery disease: Evidence from preclinical mouse models

Review

Author: Thanigaimani, Shivshankar ; Oakhill, Jonathan S ; Golledge, Jonathan ; Wesley, Callan D

BACKGROUND:

Peripheral artery disease (PAD) affects over 300 million people worldwide, causing pain, reduced mobility and impaired quality of life, and increased risk of adverse events. Currently, cilostazol is the only established medication for PAD-related leg pain. The adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway is critical in energy production, particularly in myeloid and muscle cells required for the compensatory response to limb ischemia.

METHODS:

A Systematic review and meta-analysis evaluating the effects of AMPK activation and inhibition on limb perfusion following hind limb ischemia (HLI) in mouse models was performed. The primary outcome was hind limb perfusion, and the secondary outcomes included walking distance, limb loss, capillary density and phosphorylated endothelial nitric oxide synthase (p-eNOS) levels. Twenty-five articles (401 experiment, 403 control mice) were included. Meta-analysis results were reported as standardized mean difference (SMD) or odds ratio (OR) and 95% confidence intervals (CI). Risk of bias was assessed using a tool incorporating Cochrane, ARRIVE and prior systematic review methods.

RESULTS:

AMPK activation improved hind limb perfusion (SMD 1.16, 95% CI 0.87; 1.46, p < 0.001), reduced limb loss (OR 0.30, 95% CI 0.12; 0.76, p = 0.011), and increased capillary density and p-eNOS levels. Conversely, AMPK inhibition reduced hind limb perfusion (SMD -1.50, 95% CI -2.00; -1.00, p < 0.001), and decreased capillary density and p-eNOS levels. The articles were found to have a low-to-moderate risk of bias.

CONCLUSION:

In mouse models of HLI, AMPK activation improved limb perfusion, reduced limb loss, and increased capillary density and p-eNOS levels, whereas inhibition had opposing effects. These findings support AMPK as a therapeutic target for limb ischemia.

01 Nov 2026·JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS

Processing-dependent hepatic risk and benefit of Polygonum Multiflorum Radix: Integrated chemical profiling, in vivo validation and candidate quality control markers

Article

Author: Sun, Hao ; Liu, Yanan ; Ren, Xiaoliang ; Wang, Fangyu ; Qin, Xiuping ; Liu, Meng ; Zhao, Xiaoran ; Zhang, Huijie ; Pu, Weiling ; Liang, Ying

To clarify how steaming and sun-drying cycles affect the hepatic risk-benefit profile of Polygoni Multiflori Radix (PMR), the herb was processed with black bean decoction for 1-9 cycles following the traditional "nine steaming and nine sun-drying" protocol. UPLC-MS analysis showed that anthraquinones and trans-THSG progressively decreased with increasing cycles and stabilized after five cycles, whereas cassialactone-8-O-β-D-glucoside and hyperoside emerged as new components during processing. In a low-dose LPS-sensitized mouse model mimicking immune-idiosyncratic liver injury, PMR processed for three or more cycles significantly alleviated liver damage. In an acetaminophen (APAP)-induced acute liver injury model, PMR processed for 5-7 cycles exhibited the strongest hepatoprotective effects. Spectrum-effect correlation analysis identified twelve constituents (e.g., emodin-8-O-β-D-glucoside) associated with liver injury, involving targets related to drug metabolism (CYP3A4), membrane transporters (ABCB1, SLC2A1), and oxidative stress (SOD1). Five components (e.g., cassialactone-8-O-β-D-glucoside) were linked to hepatoprotection, potentially through modulation of synthetic function (ALB) and inflammatory response (TNF, EGFR, HSP90AA1). The Cellular Thermal Shift Assay (CETSA) was employed to validate the molecular docking results, demonstrating that emodin-8-O-β-D-glucopyranoside and physcion-8-O-β-D-glucoside significantly enhanced the thermal stability of TP53. In parallel, emodin and hyperoside were confirmed to increase the thermal stability of albumin (ALB). Overall, processing PMR with black bean decoction for 5-7 cycles is optimal for reducing hepatic risk while preserving or enhancing hepatoprotective activity. These findings support a risk-benefit-oriented processing standard and propose candidate quality markers for standardized manufacturing, including trans-THSG, emodin, aloe-emodin, cassialactone-8-O-β-D-glucoside, and hyperoside.

01 Oct 2026·British Journal of Pharmacology

Pharmacogenetic mechanism of cilostazol‐induced headaches: Splicing‐mediated loss of ABCC5 gene function

Article

Author: Park, Hyun June ; Lee, Seokil ; Park, Wonhee ; Park, Joonhee ; Lee, Sung Hee ; Park, Kyungsoo ; Bang, Woo‐Dae ; Kim, Hye Won ; Cho, Sung Kweon ; Kim, Hyunho ; Lee, Ji Hyun ; Gu, Yongchul ; Hasanuzzaman, Md. ; Kim, So Won ; Lee, Jinu ; Kim, So Myoung ; Park, Danbi ; Lee, Min Goo ; Park, Yejin ; Rahaman, Md. Intazur ; Lee, Eun‐Jae ; Lee, Dong‐Hwan

Abstract:

Background and Purpose:

Cilostazol, a phosphodiesterase 3 inhibitor, causes intolerable headaches in over one third of patients, frequently leading to treatment discontinuation. We investigated whether ABCC5 variant rs7636910 (NM_005688.4:c.1146A > G) protects against cilostazol‐induced headaches through altered cyclic nucleotide signalling.

Experimental Approach:

Analysis included 101 healthy Korean volunteers from Phase 1 clinical trials, with independent replication in a multi‐ethnic cohort (n = 369) from the All of Us Research Program. Functional consequences of rs7636910 were evaluated through splicing analysis, expression studies, transport assays and cellular models examining cyclic nucleotide dynamics and vascular responses.

Key Results:

G allele carriers showed a reduced risk of moderate‐to‐severe headaches (OR = 0.29, 95% CI 0.12–0.73), replicated in the multi‐ethnic cohort (OR = 0.26, dominant model). The variant disrupted canonical splicing, causing a 38‐bp deletion, premature termination, and nonsense‐mediated decay, reducing ABCC5 expression by more than 20% in blood and thyroid tissues. Cilostazol was not an MRP5 substrate, and pharmacokinetics were genotype‐independent. In ABCC5 ‐knockdown HCASMCs (Human Coronary Artery Smooth Muscle Cells), baseline cAMP was elevated tonically with paradoxical cGMP accumulation, whereas drug‐induced cAMP fold‐increases remained comparable to controls. Tonic cAMP elevation desensitised PKA, abolishing PDE3 inhibitor‐induced vascular relaxation despite elevated cAMP—a loss recapitulated by PKA inhibition in MRP5‐normal cells.

Conclusion and Implications:

The rs7636910 variant reduces cilostazol‐induced headaches through a signalling‐based mechanism independent of drug pharmacokinetics, suggesting that transporter variants affecting endogenous substrate handling are as clinically important as drug‐metabolising enzyme polymorphisms. This variant represents a candidate pharmacogenetic biomarker for identifying cilostazol‐tolerant patients.

News (Medical) associated with Cilostazol

03 Jul 2026

·www.sciencedaily.com

The real cause of a common stroke may have been missed for decades

Scientists have discovered that a common type of stroke may have a very different cause than doctors once thought. Instead of fatty plaque clogging arteries, the strongest link was found with enlarged and damaged blood vessels deep within the brain. The finding helps explain why standard treatments like aspirin are often less effective and is driving the search for new therapies that target the brain’s tiny blood vessels directly.Scientists have uncovered evidence that could change how doctors think about a common form of stroke and why standard preventive treatments often fail. New research suggests that lacunar ischemic stroke is not primarily caused by fatty plaque building up inside arteries, as many have assumed. Instead, the strongest link appears to be with changes in the brain's blood vessels themselves, specifically the enlargement and widening of arteries. The findings may help explain why commonly prescribed stroke prevention medications such as aspirin and other antiplatelet drugs have had limited success in preventing this type of stroke. Researchers say the results are already helping guide new treatment strategies, including the LACunar Intervention Trial 3 (LACI-3), which is evaluating drugs designed to protect and support the brain's smallest blood vessels. Brain Small Vessel Disease and Stroke Risk Lacunar stroke develops when the brain's tiniest blood vessels are damaged by a condition known as small vessel disease. This form of stroke is a major cause of disability and is linked to cognitive decline, dementia, and an increased risk of future strokes. Despite its importance, scientists have struggled to pinpoint exactly what drives the disease, making it difficult to develop effective treatments. To investigate, researchers from the University of Edinburgh, the UK Dementia Research Institute, and international collaborators examined 229 people who had experienced either a lacunar stroke or a mild non-lacunar stroke. Participants received clinical and cognitive evaluations and underwent MRI brain scans shortly after their stroke and again one year later. The imaging allowed scientists to assess stroke type, monitor signs of small vessel disease, and identify any new areas of brain injury that developed over time. The team compared two different vascular changes: fatty narrowing of larger arteries and the widening and elongation of arteries within the brain. Artery Widening Emerges as a Key Clue The analysis showed that narrowing of large arteries was not associated with lacunar stroke or with small vessel disease. While artery narrowing was more common in other forms of stroke, it did not predict new brain damage on follow-up scans. In contrast, artery widening showed a strong connection to lacunar stroke. Patients with enlarged arteries were more than four times more likely to have experienced a lacunar stroke. Researchers also found that artery widening was linked to more severe small vessel disease, faster progression of brain damage, and a greater likelihood of developing new 'silent' strokes - small areas of brain tissue damage caused by interrupted blood supply that can occur without obvious symptoms. More than one in four participants developed these silent strokes during the study, even though they were receiving standard treatments intended to prevent additional strokes. New Treatment Approaches Being Tested The findings suggest that future therapies should focus on the underlying damage affecting the brain's small blood vessels rather than on fatty plaque in larger arteries. Studies such as LACI-3 are currently investigating whether existing medications, including cilostazol and isosorbide mononitrate, can help protect the brain, lower the risk of additional strokes, and reduce long-term problems involving memory, mobility, and dementia following lacunar stroke. Joanna Wardlaw, Professor of Applied Neuroimaging at the University of Edinburgh's Institute for Neuroscience and Cardiovascular Disease and Group Leader at the UK Dementia Research Institute, said: "This study provides strong evidence that lacunar stroke is not caused by fatty blockage of larger arteries, but by disease of the small vessels within the brain itself. Recognising this distinction is crucial, because it explains why conventional treatments like antiplatelet drugs are not as effective for this type of stroke and highlights the urgent need to develop new therapies that target the underlying microvascular damage." The study was published in the journal Circulation. Funding was provided by the UK Dementia Research Institute (funded by the UK Medical Research Council, Alzheimer's Society and Alzheimer's Research UK), the Leducq Foundation, the Stroke Association, British Heart Foundation, Scottish Government's Chief Scientist Office, Row Fogo Charitable Trust, Wellcome Trust, and other national funding agencies. The research team also included scientists from China and Mexico.

AHAPhase 3

16 Jun 2026

·www.einpresswire.com

Neuro-Innovators Announces Patent Application for Multi-Mechanism Stroke Recovery Platform

Patent application supports proprietary therapeutic approach designed to enhance neuroplasticity and functional recovery following neurological injury BOSTON, MA, UNITED STATES, June 16, 2026 / EINPresswire.com / -- Neuro-Innovators, Inc ., a biotechnology company advancing therapies designed to restore neurological function after injury and disease, today announced the publication of a patent application covering its multi-mechanism neurorestoration platform. The patent application expands protections for its therapeutic composition combining telmisartan, metformin, and cilostazol, three established medicines selected for their complementary effects on biological pathways associated with neuroplasticity, neurogenesis, angiogenesis, bioenergetics, remyelination, and inflammation. The platform is designed to create an environment that supports the brain's natural ability to reorganize and recover following neurological injury. Despite decades of advances in neuroscience, stroke remains a leading cause of long-term disability worldwide. Many survivors continue to experience persistent motor and cognitive impairments long after completing traditional rehabilitation programs. While many therapeutic approaches focus on individual biological targets, Neuro-Innovators has developed its platform around the belief that meaningful neurological recovery may require simultaneous support of multiple mechanisms involved in repair and adaptation. "The biology of neurologic recovery is extraordinarily complex," said J. Howison Schroeder, Chief Executive Officer of Neuro-Innovators. "When the brain begins the process of rebuilding after injury, multiple restorative pathways are active simultaneously. Our platform was designed around the concept that supporting several of these pathways at the same time may provide a more effective foundation for recovery than addressing any single mechanism in isolation." The patent application further expands Neuro-Innovators' growing intellectual property portfolio supporting its broader vision of neurorestoration, an emerging field focused on supporting the brain's capacity for adaptation and neural network reorganization following injury. The company believes neurorestoration may ultimately play an important role across a range of neurological conditions, including not only stroke, but also traumatic brain injury, and other disorders characterized by loss of neurological function. "This application represents an important step in protecting the scientific foundation underlying our neurorestoration strategy," added Schroeder. "Our long-term goal is to develop therapies that help patients recover meaningful function and improve quality of life after neurological injury." Neuro-Innovators is concurrently advancing its neurorestoration platform toward clinical evaluation in chronic stroke recovery through an investigator-initiated study at Spaulding Rehabilitation Hospital. About Neuro-Innovators Neuro-Innovators is a first in class clinical-stage pharmaceutical company focused on developing compound therapies designed to support biological pathways associated with neurological recovery following stroke, brain injury, and other neurological conditions. The company’s mission is to improve functional outcomes for patients while reducing the long-term personal and societal burden of neurologic disability. Healing Brains with Neuroplastic Medicine™ For more information, please visit www.neuro-innovators.com and follow Neuro-Innovators on LinkedIn . Media Contact Madelyn De Los Santos Putnam Insights LLC madelyn@putnaminsights.com Legal Disclaimer: EIN Presswire provides this news content "as is" without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the author above.

28 May 2024

·www.prnewswire.com

Genovate Announces Plans to Submit a New Drug Application for PMR to the U.S. Food & Drug Administration in the Second Half of 2025

TAIPEI, May 28, 2024 /PRNewswire/ -- Genovate Biotechnology Co., Ltd. (TPEx: 4130), a Taiwan-based specialty pharmaceutical company, today announced its plans to submit a New Drug Application (NDA) with the United States Food and Drug Administration (US FDA) for PMR, an investigational once daily extended-release form of cilostazol for the treatment of Intermittent Claudication, in the second half of 2025. In the written responses to the pre-NDA meeting package, the FDA confirmed that the clinical studies conducted are sufficient to support the submission of a marketing application under the 505(b)(2) regulatory pathway. The key study in the submission package, GBL23-001 (NCT06167265), is a randomized, fully replicate crossover study designed to evaluate the bioequivalence and within-subject variability between PMR 145 mg once daily and the immediate-release tablet of cilostazol 100 mg twice daily. This study is expected to be completed in mid-2024, and the top-line results have shown that the primary endpoints of the study were achieved, and the decision to submit the application was made following the successful outcome of study GBL23-001. Furthermore, Genovate has been improving the PMR formulation and its manufacturing processes in order to address additional FDA comments. All clinical study and manufacturing data are expected to be included in the final submission package. "We are pleased to share what we believe is an efficient regulatory pathway for PMR with the goal of bringing a new treatment option to the people who suffer from intermittent claudication and recurrence of cerebral infarction, from the US to the globe." said Chia-Chen Chu, General Manager of Genovate. About PMR (Cilostazol Extended-Release Tablets) PMR, a novel extended-release (ER) formulation of cilostazol, was designed to reduce the concentration-dependent side effects associated with immediate-release (IR) tablet form of cilostazol. Cilostazol is currently available in IR tablet form at 50 and 100 mg strengths administered twice daily. The IR formulation of cilostazol, marketed as Pletal® in the US (Pletaal® in Taiwan and other Asian countries), was first available in Japan in 1988 for the treatment of peripheral arterial diseases and the prevention of recurrence of cerebral infarction and later approved by the US FDA in 1999 for the treatment of intermittent claudication (IC). Cilostazol is a specific PDE III inhibitor that can cause reduced platelet aggregation and increased vasodilatation. Cilostazol showed good efficacy in preventing secondary strokes, notably reducing the rates of ischaemic stroke recurrence. Nevertheless, the results from eight placebo-controlled clinical trials indicated that 15.4% of patients withdrawn from cilostazol treatment were as a result of adverse reactions. Headache, palpitations, and diarrhea were the most frequently reported adverse reactions among these patients. These adverse reactions were attributable to the peak concentration of cilostazol. Genovate is developing an ER tablet form of cilostazol, PMR, to be administered once daily aiming to improve adherence and to reduce the side effects associated with the high peak-to-trough variation of the concentration of cilostazol IR. About Intermittent Claudication Peripheral arterial disease (PAD) affects over 200 million people globally and around 8.5 million Americans over the age of 40. PAD occurs as a result of the narrowing or blockade of blood vessels that carry blood from the heart to the legs. The main symptom of PAD observed in approximately 70% of patients is intermittent claudication (IC), a condition that presents as pain and cramping in the lower extremities (thigh, calf, hip and buttock muscles), as a result of limited blood flow. IC is commonly viewed as a signal of substantial atherosclerosis, suggesting a higher likelihood of heart attack or stroke. The symptoms of IC are intermittent, exacerbated when walking or during exercise, and are alleviated with rest, but reoccur when activity resume; as a result, IC can be very debilitating, drastically affecting the quality of life of those affected. In severe cases, IC may require surgical intervention, but in general, it can be treated and managed with a combinational approach including medication, life style changes that modify or eliminate risk factors, and exercise program. Drugs improving blood flow such as anti-clotting agents (aspirin), anti-hypertensives, statins, and phosphodiesterase (PDE) III inhibitors such as cilostazol are currently used to treat IC. About Genovate Biotechnology Co., Ltd. Genovate Biotechnology Co., Ltd. is a Taiwan-based, fully integrated specialty pharmaceutical company focusing on the new drug development in new formulation, new active ingredient, new treatment modality in cardiovascular, autoimmune, neurodegenerative, and liver diseases. Genovate is equipped with PIC/S GMP manufacturing, marketing, and distribution capabilities. Forward-Looking Statements All statements other than statements of historical facts contained in this press release are forward-looking statements, including statements regarding the timing of any regulatory process or ultimate approvals for PMR for the treatment of IC. These forward-looking statements speak only as of the date of this press release and are subject to a number of risks, uncertainties and assumptions, including the risks and uncertainties associated with the projected timeline of our NDA submission, whether FDA will agree with our interpretation of the data or the adequacy of data to support an NDA, the FDA's review of our NDA, market conditions, as well as risks and uncertainties inherent in Genovate's business. The events and circumstances reflected in the company's forward-looking statements may not be achieved or occur and actual results could differ materially from those projected in the forward-looking statements. Except as required by applicable law, the company does not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise. SOURCE Genovate Biotech

Drug ApprovalClinical ResultNDA

100 Deals associated with Cilostazol

External Link

KEGG	Wiki	ATC	Drug Bank
D01896	Cilostazol	B01AC23	DB01166

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Brain Infarction	Japan	Otsuka Pharmaceutical Co., Ltd.	15 Mar 2007
Peripheral Vascular Diseases	Brazil	Libbs Farmacêutica Ltda.	05 Jun 2002
Stroke	Brazil	Libbs Farmacêutica Ltda.	05 Jun 2002
Intermittent Claudication	United States	Otsuka Pharmaceutical Co., Ltd.	15 Jan 1999
Arterial Occlusive Diseases	China	Zhejiang Otsuka Pharmaceutical Co. Ltd.	01 Jan 1996

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Angina Pectoris, Variant	Phase 3	South Korea	Korea Otsuka Pharmaceutical Co., Ltd.	01 Nov 2013
Acrodynia	Phase 1	China	Sichuan Xuhui Pharmaceutical Co., Ltd.	22 Jul 2026
Ischemia	Phase 1	China	Sichuan Xuhui Pharmaceutical Co., Ltd.	22 Jul 2026
Occlusion of artery	Phase 1	China	Sichuan Xuhui Pharmaceutical Co., Ltd.	22 Jul 2026
Ulcer	Phase 1	China	Sichuan Xuhui Pharmaceutical Co., Ltd.	22 Jul 2026
Tinnitus	Clinical	South Korea	Korea Otsuka Pharmaceutical Co., Ltd.	01 Jul 2011
Chemical and Drug Induced Liver Injury	Preclinical	Egypt	Badr University In Cairo	09 Apr 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESC2025	Not Applicable	Lower limb ischemia	844	Cilostazol alone	qyqvbqwgzs(ywmkjkjgmo): HR = 0.84 (95.0% CI, 0.68 - 1.03), P-Value = 0.09 View more	Positive	30 Aug 2025
				Aspirin or clopidogrel
NCT06242145 (Pubmed \| Neurol Sci)	Phase 3	Acute Ischemic Stroke	580	Cilostazol	enxspsvwmy(lizyxccjni) = ayjtpvqxoo idtgfunzwt (pfgtupjslk )	Positive	15 Apr 2025
				Clopidogrel	enxspsvwmy(lizyxccjni) = tpdgnwuevo idtgfunzwt (pfgtupjslk )
NCT06242132 (CILO-CLOP Trial, Pubmed \| Neurol Ther)	Phase 3	Acute Ischemic Stroke hypertension	870	Cilostazol	trdtshpjuv(ezfwxvxboz) = imqhtzqxku qotdrhlxja (zwcelizjae )	Positive	12 Apr 2025
				Clopidogrel	trdtshpjuv(ezfwxvxboz) = opcrjaugvi qotdrhlxja (zwcelizjae )
NCT05126836 (CLIP-HFpEF, Pubmed \| ESC Heart Fail)	Phase 2	Heart Failure, Diastolic	23	Cilostazol	jqzvofopfj(cmqfcsikzi) = kxhudhufhk ydskgrqmno (dbhbxwvmew, 68 - 974) View more	Positive	01 Apr 2025
				Placebo	jqzvofopfj(cmqfcsikzi) = mcozfkeytb ydskgrqmno (dbhbxwvmew, 154 - 1056) View more
NCT01261234 (Randomized Controlled Trial of Cilostazol Addition for In-Stent Restenosis After Carotid Artery Stenting, Pubmed \| Stroke)	Not Applicable	Vascular restenosis	631	Cilostazol 50 mg	unzrcapggk(mccryjqtwr) = fvdquanmdq gcxvuyfqmh (axshednxac ) View more	Positive	01 Dec 2024
				No Cilostazol	unzrcapggk(mccryjqtwr) = kvjrsghnec gcxvuyfqmh (axshednxac ) View more
NCT05126836 (CLIP-HFpEF, Pubmed \| ESC Heart Fail)	Phase 2	Heart Failure, Diastolic	23	Cilostazol	ohxrwqchcy(syegbqzoir) = zipzijmypx wxacnyppev (spzzbvwdqa, 68 - 974) View more	Positive	17 Nov 2024
				Placebo	ohxrwqchcy(syegbqzoir) = bmdgyfznvz wxacnyppev (spzzbvwdqa, 154 - 1056) View more
NCT03451591 (LACI-2, CTgov)	Phase 2/3	Stroke, Lacunar	363	Isosorbide Mononitrate (Isosorbide Mononitrate XL (ISMN))	chlsvoalre = soqftsabkn himsxqwjts (rklnqtjouy, sglstredcl - subdpnyasb) View more	-	12 Nov 2024
				Cilostazol (Cilostazol)	chlsvoalre = xajybuvxxd himsxqwjts (rklnqtjouy, loccjepewl - uihfjrftng) View more
NCT05126836 (CLIP-HFpEF, CTgov)	Phase 2	Heart failure with normal ejection fraction \| Heart Failure, Diastolic	25	Placebo+Cilostazol 100Mg Tab (Cilostazol)	tftofgcfff(djtgkhvztc) = mizfytoobs nhxxyhunqa (jizenjvfwy, yozskblrnj - tqnhpqrvyn) View more	-	15 Dec 2023
				Placebo+Cilostazol 100Mg Tab (Placebo)	tftofgcfff(djtgkhvztc) = brievfuufv nhxxyhunqa (jizenjvfwy, zcafcdwwsq - qdxyndbijx) View more
ESC2023	Phase 4	ST Elevation Myocardial Infarction	985	DAT (aspirin and clopidogrel for 12 months)	pqyrqlszus(vzitvzhnfi) = vdzfkdkgzt fpjbljsrlg (audlhkeikt )	Negative	25 Aug 2023
				TAT 1M (aspirin, clopidogrel, and cilostazol for 1 month)	pqyrqlszus(vzitvzhnfi) = svgpsibuab fpjbljsrlg (audlhkeikt )
NCT01995370 (CSPS.com, Pubmed \| Stroke)	Phase 4	Stroke, Lacunar	925	DAPT group receiving cilostazol and either aspirin or clopidogrel	nonowvjfph(robjzljqev) = mgnldiqpow chlmsnlrhz (rxbryvxtlu )	Positive	03 Feb 2023
				SAPT group receiving aspirin or clopidogrel alone	nonowvjfph(robjzljqev) = ihnkhqjihr chlmsnlrhz (rxbryvxtlu )

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