A Phase 4, Open-label, Blinded Primary Endpoint, Randomized Multicenter Trial to Assess the Effectiveness of Evolocumab With Routine Lipid Management Compared With Routine Lipid Management Alone in Reducing the Plaque Burden in Patients With Subclinical Atheroma

The main aim of this trial is to demonstrate that Evolocumab plus routine lipid management is superior to routine lipid management alone in modifying plaque (non-calcified) volume as measured by Artificial Intelligence-enabled Quantitative Coronary Plaque Analysis (AI-QCPA) from Coronary Computed Tomography Angiography (CCTA).

Start Date31 Jan 2027

Sponsor / Collaborator

Amgen, Inc.

NCT06081153

/ Not yet recruitingEarly Phase 1IIT

A Randomized, Placebo-Controlled Mechanistic Clinical Trial of PCSK9 Inhibition With Evolocumab in Patients Undergoing Open Abdominal Aortic Aneurysm Repair

The goal of this mechanistic clinical trial is to assess whether lowering the low-density lipoprotein cholesterol (LDL-C) levels in the blood with the injections of the medication evolocumab will have any effect on the tissue or cells of patients with abdominal aortic aneurysm (AAA). Researchers will compare participants receiving evolocumab injections to participants receiving placebo injections to see how the tissue and cells of the aorta are affected by changes in LDL-C levels.

Start Date01 Dec 2026

Sponsor / Collaborator

University of Pennsylvania

[+2]

ChiCTR2600130261

/ Not yet recruitingPhase 4IIT

Clinical Study of PCSK9 Inhibitors for Preventing Early Neurological Deterioration in Branch Atheromatous Disease

Start Date07 Aug 2026

Sponsor / Collaborator

First Affiliated Hospital of Dalian Medical University

100 Clinical Results associated with Evolocumab

100 Translational Medicine associated with Evolocumab

100 Patents (Medical) associated with Evolocumab

672

Literatures (Medical) associated with Evolocumab

01 Dec 2026·International journal of cardiology. Cardiovascular risk and prevention

Comment on “Lipoprotein(a) reduction with inclisiran, alirocumab, evolocumab, enlicitide, and lerodalcibep: A systematic review and meta-analysis of randomized controlled trials”

Letter

Author: Paul, Jeffrin Reneus ; Shridevi, Kotina ; Ratnakar, Parag J ; Gupta, Vatsala ; Gaurav

01 Nov 2026·AMERICAN JOURNAL OF OPHTHALMOLOGY

Epidemiology, Safety of Dilation, and Medication-Associated Risk of Acute Angle-Closure Crisis in the United States

Article

Author: Schultz, Jeffrey S ; Shah, Jainam ; Adamovich-Zeitlin, Richard ; Oseni, Jessinta ; Berdahl, John P ; Shrivastava, Anurag ; Ong, Joshua ; Pathuri, Sachin

OBJECTIVE:

To evaluate the epidemiology of acute angle-closure crisis (AACC), the safety of pharmacologic dilation, and medication-associated AACC risk in the United States.

DESIGN:

Retrospective clinical cohort study.

SUBJECTS:

Adults (≥18 years) in a multicenter federated electronic health record network.

METHODS:

Using deidentified electronic medical record data from 2010 to 2025, AACC cases were identified using ICD-10-CM codes followed by definitive therapeutic intervention within 14 days. Incidence, prevalence, and diagnostic trends were evaluated with Mann-Kendall tests. Dilation-associated AACC risk was assessed among patients undergoing dilation-associated ophthalmic examinations, with incident AACC identified within 14 days (with 24-hour sensitivity analysis). Medication-associated AACC risk was evaluated using active-comparator cohorts with 1:1 propensity score matching and Cox proportional hazards models over a 30-day window.

MAIN OUTCOME MEASURES:

AACC incidence (per 100,000 dilation-associated examinations) and hazard ratios (HRs) with 95% confidence intervals (CIs) for medication-associated AACC risk.

RESULTS:

From 2010 to 2025, the cumulative incidence of AACC was 0.014%, and the prevalence of primary angle-closure glaucoma (PACG) among patients with AACC was 16.7%. AACC incidence and the prevalence of PACG among patients with AACC increased over time (all P < .001). Gonioscopy utilization declined, whereas anterior segment imaging increased (all P < .001). Across 3,400,372 dilation-associated examinations among 2,444,570 patients, post-dilation AACC was rare (3.1 per 100,000; 95% CI: 2.3-3.7), with similar findings in a 24-hour sensitivity analysis; events concentrated among patients with anatomical risk factors. Increased AACC risk was observed for medications with established associations and some with less established associations, including lactulose (HR: 1.67), metoclopramide (1.38), sumatriptan (1.64), prazosin (1.32), and terazosin (1.77) (all P < .05). Previously unreported associations were observed for calcitonin gene-related peptide (CGRP) monoclonal antibodies (erenumab [1.33]), calcium channel blockers (CCBs) (verapamil [1.89], diltiazem [1.74]), and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (alirocumab [1.54], evolocumab [1.46]) (all P < .05).

CONCLUSIONS:

AACC following pharmacologic dilation was rare and occurred predominantly among anatomically predisposed patients, supporting the safety of dilation in routine care. Medication-associated risk signals highlight the importance of proactive ocular risk assessment and medication reconciliation. Novel associations with CCBs, CGRP monoclonal antibodies, and PCSK9 inhibitors warrant further investigation.

01 Nov 2026·Endocrinology, diabetes & metabolism

Impact of Evolocumab on LDL‐Cholesterol and Cardiovascular Outcomes in Patients With Established CVD: Systematic Review and Meta‐Analysis

Review

Author: Naveed, Muhammad Abdullah ; Reddy, K. Sai Varun ; Awashra, Ameer ; Verma, Amogh ; Chauhan, Anchit ; Maloth, Arun Kumar ; Mahmood, Affaf ; Mukhlis, Muhammad ; Tahir, Haris Bin ; Goel, Anika ; Tandel, Hemeesh

ABSTRACT:

Background:

Atherosclerotic cardiovascular disease is a leading cause of morbidity and mortality, and many high‐risk patients fail to reach LDL‐cholesterol (LDL‐C) targets on statins alone. Evolocumab, a PCSK9 inhibitor, offers potent LDL‐C lowering, but a synthesis of its lipid and clinical benefits in secondary prevention is needed.

Methods:

We conducted a systematic review and meta‐analysis of randomised controlled trials evaluating evolocumab in adults with established cardiovascular disease. PubMed, Embase, Scopus, Cochrane CENTRAL, and ClinicalTrials.gov were searched through April 2025. Outcomes included lipid parameters, major adverse cardiovascular events (MACE), individual cardiovascular endpoints, and safety, with pooled risk ratios (RR) and mean differences calculated using random‐effects models.

Results:

Nine trials enrolling 67,662 patients were included. Evolocumab significantly reduced LDL‐C (mean difference −57.73 mg/dL), total cholesterol (−52.27 mg/dL), triglycerides (−21.21 mg/dL), and lipoprotein(a) (−10.99 mg/dL), while increasing HDL‐cholesterol (3.69 mg/dL). Evolocumab was associated with lower MACE (RR 0.53; 95% CI 0.40–0.71), though this estimate should be interpreted cautiously given heterogeneity in endpoint definitions and study designs. Myocardial infarction (RR 0.74) and coronary revascularisation (RR 0.80) were significantly reduced, while cardiovascular mortality and stroke showed no statistically definitive reduction. Serious adverse events and neurocognitive effects were comparable between groups, though injection‐site reactions were more frequent with evolocumab.

Conclusion:

In patients with established cardiovascular disease, evolocumab provides substantial lipid lowering and reduces ischemic events without major safety concerns, supporting its use as an adjunct to statin therapy in secondary prevention.

277

News (Medical) associated with Evolocumab

20 Oct 2026

·www.inhibikase.com

Inhibikase Therapeutics Appoints Scott Wasserman to Board of Directors

WILMINGTON, Del., Oct. 20, 2026 (GLOBE NEWSWIRE) -- Inhibikase Therapeutics, Inc. (Nasdaq: IKT) (“Inhibikase” or “Company”), a clinical-stage pharmaceutical company developing IKT-001, a novel once-daily oral anti-proliferative for Pulmonary Arterial Hypertension (“PAH”), today announced the appointment of Scott M. Wasserman, MD, to the Company’s Board of Directors, effective October 19, 2026. Concurrent with Dr. Wasserman’s appointment, the Company also announced the resignation of Dennis Berman from the Company’s Board. “We thank Dennis for his many contributions to the Company during his years of service,” said Amit Munshi, Chair of the Inhibikase Board of Directors. Dr. Wasserman is currently the Chief Medical Officer of Kailera Therapeutics, a clinical-stage company developing GLP-1-based therapeutics for obesity and related conditions. Dr. Wasserman is a cardiologist with more than two decades of experience in clinical development and company leadership. At Amgen Inc., he served as Vice President, Global Development and Therapeutic Area Head for Bone, Cardiovascular, Metabolic and Neuroscience. He was Amgen’s first cardiologist and built the company’s cardiovascular and metabolic strategy, team and portfolio. He led the global development and approvals of Repatha (evolocumab), was instrumental in the development and U.S. FDA approval of Evenity (romosozumab) and oversaw the U.S. approval of Aimovig (erenumab). “Scott has taken multiple programs from early development through global approval, and he has built clinical organizations at both large and emerging companies,” said Amit Munshi. “We look forward to benefiting from his expertise as we continue to advance our global Phase 3 IMPROVE-PAH study of IKT-001. We are pleased to welcome Scott to our Board. “PAH is a progressive, life-threatening disease, and the pedigree of imatinib together with the recent preclinical and Phase 1 data for IKT-001 point to a very promising role for this asset in this difficult to treat condition,” said Dr. Wasserman. “This is an important time for Inhibikase, and I look forward to applying my experience in global clinical development and regulatory interactions as the Company advances IMPROVE-PAH.” Scott brings deep expertise in clinical development to Inhibikase’s Board of Directors, spanning global development strategy, clinical trial design and execution, and global regulatory interactions. Most recently, Scott served as Venture Partner at Frazier Life Sciences, focusing on company creation. Prior to Frazier, Scott was the CEO and co-founder of Latigo Biotherapeutics, a venture-backed biotechnology company developing first and best-in-class, non-opioid pain medicines. Prior to his role with Latigo, Scott was Vice President, Global Development Therapeutic Area Head for Bone, Cardiovascular, Metabolic, and Neuroscience at Amgen. In addition to his role in the development of Repatha, Evenity, and Aimovig, Scott oversaw therapeutic development for a range of other conditions, including heart failure, anemia, obesity, and Alzheimer’s disease. Prior to joining industry, Scott was on faculty at Stanford University in the Division of Cardiovascular Medicine conducting NIH-sponsored research on endothelial gene expression and served as a non-interventional cardiologist at the Veterans Administration Hospital in Palo Alto, CA. Scott received his BS, Magna Cum Laude from Haverford College and his MD, Magna Cum Laude from Harvard Medical School. He completed his postgraduate training in Internal Medicine and Cardiovascular Medicine at Stanford University and post-doctoral cardiovascular research at COR Therapeutics, Millennium Pharmaceuticals, and Stanford. About Inhibikase (www.inhibikase.com) Inhibikase Therapeutics, Inc. (Nasdaq: IKT) is a clinical-stage pharmaceutical company developing therapeutics to modify the course of cardiopulmonary diseases, namely, Pulmonary Arterial Hypertension (“PAH”), in which aberrant signaling through type III receptor tyrosine kinases, including platelet derived growth factor receptors and a stem cell factor receptor, known as “c-Kit,” has been implicated. Our lead product candidate is IKT-001, a prodrug of imatinib mesylate (“imatinib”), for PAH which is an orphan indication. Imatinib was first approved in the United States in 2001 for various cancers and blood disorders and, following more than 20 years of clinical use, has a well-characterized safety profile with the first reported use of imatinib in PAH occurring in 2005. PAH is a progressive, life-threatening disease characterized by pulmonary vascular remodeling and elevated pulmonary vascular resistance that affects approximately 50,000 Americans. Our single pivotal Phase 3 clinical study in PAH in approximately 180 sites around the world, named IMPROVE-PAH (IKT-001 for Measuring Pulmonary Vascular Resistance and Outcome Variables in a Phase 3 Evaluation of PAH), is actively enrolling patients. Social Media Disclaimer Investors and others should note that the Company announces material financial information to investors using its investor relations website, press releases, SEC filings and public conference calls and webcasts. The Company intends to also use LinkedIn as a means of disclosing information about the Company, its services and other matters and for complying with its disclosure obligations under Regulation FD. Forward-Looking Statements This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking terminology such as “believes,” “expects,” “may,” “will,” “should,” “anticipates,” “plans,” or similar expressions or the negative of these terms and similar expressions are intended to identify forward-looking statements. These forward-looking statements include, but are not limited to, statements regarding the potential of IKT-001, the advancement of the IMPROVE-PAH study, and the anticipated contribution of Dr. Wasserman to the Company's board of directors. These forward-looking statements are based on Inhibikase’s current expectations and assumptions. Such statements are subject to certain risks and uncertainties, which could cause Inhibikase’s actual results to differ materially from those anticipated by the forward-looking statements. Important factors that could cause actual results to differ materially from those in the forward-looking statements include our ability to execute a Phase 3 study to evaluate IKT-001 as a treatment for PAH, as well as such other factors that are included in our periodic reports on Form 10-K and Form 10-Q that we file with the U.S. Securities and Exchange Commission. Any forward-looking statement in this release speaks only as of the date of this release. Inhibikase undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future developments or otherwise, except as may be required by any applicable securities laws. Contacts: Investor Relations: Michael Moyer LifeSci Advisors mmoyer@lifesciadvisors.com Released October 20, 2026

Drug ApprovalExecutive ChangePhase 1Phase 3

10 Sep 2026

·www.biospace.com

Moonwalk Biosciences Announces $70 Million Series B Financing to Advance Adipose-Targeted RNAi Therapies for Obesity and Cardiometabolic Diseases

Financing co-led by Alpha Wave and YK Bioventures, with participation from Eli Lilly and Company, Gaorong Ventures and existing investors ARCH Venture Partners, Khosla Ventures and Future Ventures Proceeds will advance Moonwalk's lead obesity program into the clinic and accelerate a pipeline of adipose-selective RNAi medicines targeting novel biology Dr. Stephen Djedjos appointed Senior Vice President, Clinical Development Moonwalk Biosciences , a biotechnology company developing first-in-class adipose-targeted RNA interference (RNAi) medicines for obesity and cardiometabolic diseases, today announced the closing of an oversubscribed $70 million Series B financing. The financing was co-led by Alpha Wave and YK Bioventures, with participation from Eli Lilly and Company, Gaorong Ventures, and existing investors ARCH Venture Partners, Khosla Ventures and Future Ventures. Proceeds will support advancement of Moonwalk's lead obesity candidate, MW101, into first-in-human clinical studies in late 2027, expand the Company's pipeline of tissue-targeted siRNA medicines and further advance its proprietary discovery platform. Moonwalk's programs are designed to selectively deliver siRNA therapeutics directly to adipose tissue, enabling precise modulation of novel, non-incretin pathways underlying obesity. The Company's differentiated approach combines human genetics, epigenomics and multi-omics discovery with proprietary tissue-targeting chemistry to unlock previously inaccessible biology and develop first-in-class medicines with the potential for durable efficacy, preservation of lean muscle mass and infrequent dosing. The platform enables highly specific modulation of adipose biology while minimizing effects on other tissues. Moonwalk exclusively licensed the adipose-targeting chemistry from Suzhou Siran Biotechnology Co., Ltd. for its first-in-class pipeline, which focuses on modulating novel pathways involved in energy homeostasis, adipogenesis, lipolysis and thermogenesis. “Obesity places an extraordinary physical and emotional burden on millions of people,” said Alex Aravanis, M.D., Ph.D., CEO & Co-Founder, Moonwalk Biosciences. “This financing brings us closer to developing a new generation of adipose-targeted medicines designed to improve outcomes for people living with obesity and related cardiometabolic diseases.” “Obesity is one of the most significant global health challenges, and Moonwalk is pursuing a fundamentally different approach to treating it,” said Rick Gerson, co-founder, Chairman and CEO of Alpha Wave Global. “By targeting adipose tissue directly, Moonwalk may redefine how obesity is treated by delivering therapies with the potential for durable efficacy, lean muscle preservation and infrequent dosing.” “What stood out to us about Moonwalk is the depth of the science behind the platform and the strength of the preclinical evidence generated to date,” said Chris Dimitropoulos, Managing Director, Life Sciences Investments of Alpha Wave Global. “By combining adipose-selective RNAi delivery with human genetics, epigenomics and multi-omics discovery, the Moonwalk team has devised a highly precise way to modulate adipose biology.” In addition to the financing, Dr. Stephen Djedjos has been appointed as Senior Vice President, Clinical Development at Moonwalk, bringing more than 20 years of clinical and drug development experience. Most recently, he served as SVP and Head of Clinical Development at Kailera Therapeutics, where he led clinical development as the company advanced its incretin therapies for obesity and metabolic diseases. Previously, he held senior clinical development roles at Mineralys Therapeutics, Sana Biotechnology, Gilead Sciences and Amgen, where he contributed to the development and approval of Repatha®. A physician and pediatric endocrinologist by training, Dr. Djedjos completed his fellowship at Johns Hopkins Hospital. Across multiple preclinical studies, Moonwalk has demonstrated robust reductions in body weight and fat mass while preserving lean muscle mass without reducing food intake. The Company has also generated translational evidence demonstrating favorable modulation of metabolic pathways consistent with healthy adipose remodeling. In non-human primate studies, Moonwalk demonstrated durable adipose target engagement following a single dose, supporting the potential for quarterly or twice-yearly dosing. Moonwalk's lead development candidate, MW101, is expected to enter first-in-human clinical studies in late 2027 following completion of ongoing IND-enabling studies. In parallel, the Company is advancing multiple additional tissue-targeted siRNA programs for obesity and cardiometabolic diseases. Moonwalk Biosciences is developing first-in-class adipose-targeted RNA interference (RNAi) medicines for obesity and cardiometabolic diseases. The Company's proprietary AI-enabled discovery platform integrates human genetics, epigenomics and multi-omics with adipose-selective siRNA chemistry to identify and validate novel therapeutic targets involved in adipose biology, without affecting appetite. Moonwalk is advancing a pipeline of therapies designed to preserve lean mass, improve tolerability and enable infrequent dosing while addressing the underlying biology of obesity and metabolic disease. The content above comes from the network. if any infringement, please contact us to modify.

Executive Change

09 Sep 2026

·www.sciencedaily.com

DNA treatment cuts bad cholesterol by nearly 50% without statins

Researchers have designed a new DNA-based treatment that targets PCSK9, a protein closely tied to high LDL cholesterol and atherosclerosis. Their most effective molecule reduced PCSK9 protein by 87% in human liver cells and lowered cholesterol by 47% in genetically modified mice after a single injection.High cholesterol can quietly damage arteries for years, raising the risk of heart disease and other cardiovascular problems. Now, researchers from the University of Barcelona and the University of Oregon have developed an experimental strategy that could offer a new way to bring cholesterol levels down. The approach targets PCSK9, a protein that plays a major role in controlling levels of low-density lipoprotein cholesterol (LDL-C), often called "bad" cholesterol. By suppressing PCSK9, the treatment helps cells remove more cholesterol from the bloodstream, potentially reducing the buildup of fatty plaques inside arteries that can lead to atherosclerosis. Instead of relying on statins, the researchers used molecules called polypurine hairpins (PPRH). These specially designed DNA molecules can interfere with the activity of specific genes. In this case, they were used to reduce production of PCSK9. The findings were published in the journal Biochemical Pharmacology. The research was led by Carles J. Ciudad and Verònica Noé, professors at the University of Barcelona's Faculty of Pharmacy and Food Sciences and the Institute of Nanoscience and Nanotechnology (IN2UB), together with Nathalie Pamir of the University of Oregon in Portland (United States). The work was supported by projects from the Spanish Ministry of Science, Innovation and Universities (MICINN) and the National Institutes of Health (NIH) of the United States. Targeting a Key Cholesterol Protein PCSK9 (protein convertase subtilisin/kexin type 9) has become an important target in cardiovascular medicine over the past decade because of its influence on cholesterol metabolism. Cells use LDL receptors to capture LDL cholesterol circulating in the blood. PCSK9 interferes with this process by reducing the number of LDL receptors available on the cell surface. With fewer receptors available to remove cholesterol, more LDL cholesterol remains in the bloodstream, contributing to hypercholesterolemia. The new strategy attempts to stop that process closer to its source by reducing expression of the PCSK9 gene itself. Polypurine hairpins (PPRHs) are short, single-stranded DNA molecules known as oligonucleotides. They are designed to recognize and bind very specific DNA or RNA sequences. Once attached to their target, they can interfere with gene transcription, the process cells use to make RNA from DNA instructions. In this study, researchers tested two PPRHs, called HpE9 and HpE12. Both reduced PCSK9 RNA and protein while increasing levels of LDLR, the receptor that helps cells take up LDL cholesterol. "Specifically, one of the arms of each chain of the HpE9 and HpE12 polypurines binds specifically to polypyrimidine sequences of exons 9 and 12 of PCSK9, respectively, via Watson-Crick bonds," notes Professor Carles J. Ciudad, from the Department of Biochemistry and Physiology. That binding interferes with transcription of the gene, either by disrupting the activity of RNA polymerase, the enzyme that produces RNA, or by preventing transcription factors from attaching to DNA. Cholesterol Fell 47% in Mice The researchers also tested the technique in vivo using transgenic mice engineered to express the human PCSK9 gene. The strongest results came from HpE12. "The results show that both HpE9 and HpE12 are highly effective in HepG2 cells. HpE12 decreases PCSK9 RNA levels by 74% and protein levels by 87%. In the case of transgenic mice, a single injection of HpE12 reduces plasma PCSK9 levels by 50% and cholesterol levels by 47% on the third day," says Professor Verònica Noé. The findings suggest that suppressing PCSK9 with PPRHs can increase the availability of LDL receptors and help cells pull more cholesterol out of circulation. In principle, that could reduce the amount of cholesterol available to contribute to plaque formation in artery walls. Because the cholesterol reduction was demonstrated in mice, however, additional research would be needed to determine whether the approach is safe and effective in humans. A Potential Alternative to Existing Cholesterol Drugs PCSK9 is already the target of several cholesterol-lowering therapies. Researchers have explored gene silencing approaches using siRNAs, antisense oligonucleotides, and CRISPR. Inclisiran, for example, is an siRNA-based medication that reduces production of PCSK9. Monoclonal antibodies such as evolocumab and alirocumab also target the protein. The researchers argue that PPRHs could offer another option. They say these molecules may have several practical advantages, including relatively inexpensive production, stability and a low likelihood of provoking an immune response. "PPRHs, especially HpE12, are therapeutic oligonucleotides with many advantages, including low cost of synthesis, stability and lack of immunogenicity. In addition, such a PPRH-based approach against PCSK9 would not lead to side effects such as the myopathies associated with statin therapy," the experts conclude. If future studies confirm the findings in people, targeting PCSK9 with polypurine hairpins could eventually add another tool to the growing range of treatments designed to lower LDL cholesterol and protect cardiovascular health.

Clinical ResultOligonucleotide

100 Deals associated with Evolocumab

External Link

KEGG	Wiki	ATC	Drug Bank
D10557	Evolocumab	C10AX13	DB09303

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Coronary Disease	China	Amgen, Inc.	14 Feb 2019
Hypercholesterolemia	Japan	Amgen KK	22 Jan 2016
Hypercholesterolemia, Familial	Japan	Amgen KK	22 Jan 2016
Heterozygous familial hypercholesterolemia	United States	Amgen, Inc.	27 Aug 2015
Primary Hyperlipidemia	United States	Amgen, Inc.	27 Aug 2015
Atherosclerosis	European Union	Amgen Europe BV	17 Jul 2015
Atherosclerosis	Iceland	Amgen Europe BV	17 Jul 2015
Atherosclerosis	Liechtenstein	Amgen Europe BV	17 Jul 2015
Atherosclerosis	Norway	Amgen Europe BV	17 Jul 2015
Atherosclerosis	United Kingdom	Amgen Ltd.	17 Jul 2015
Complex dyslipidemia	European Union	Amgen Europe BV	17 Jul 2015
Complex dyslipidemia	Iceland	Amgen Europe BV	17 Jul 2015
Complex dyslipidemia	Liechtenstein	Amgen Europe BV	17 Jul 2015
Complex dyslipidemia	Norway	Amgen Europe BV	17 Jul 2015
Complex dyslipidemia	United Kingdom	Amgen Ltd.	17 Jul 2015
Homozygous familial hypercholesterolemia	European Union	Amgen Europe BV	17 Jul 2015
Homozygous familial hypercholesterolemia	Iceland	Amgen Europe BV	17 Jul 2015
Homozygous familial hypercholesterolemia	Liechtenstein	Amgen Europe BV	17 Jul 2015
Homozygous familial hypercholesterolemia	Norway	Amgen Europe BV	17 Jul 2015
Homozygous familial hypercholesterolemia	United Kingdom	Amgen Ltd.	17 Jul 2015

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Calcification of coronary artery	Phase 3	United States	Amgen, Inc.	19 Mar 2019
Coronary Artery Disease	Phase 3	United States	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Australia	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Czechia	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Germany	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Hungary	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Italy	Amgen, Inc.	19 Nov 2018
Coronary Artery Disease	Phase 3	Netherlands	Amgen, Inc.	19 Nov 2018
Acute Coronary Syndrome	Phase 3	Switzerland	Amgen, Inc.	23 Jan 2018
Arteritis	Phase 3	United States	Amgen, Inc.	14 Apr 2016

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ACTRN12622001003763 (ESMO2026)	Phase 2	Metastatic castration-resistant prostate cancer PCPro-positive	15	Evolocumab + Evolocumabherapy	dgeuquwjor(kbcfdcmdvw) = xagzgecume hijoddvivh (pfaamtpgor )	Negative	23 Oct 2026
NCT06284564 (BOOST-RCC, ESMO2026)	Phase 2	Metastatic Renal Cell Carcinoma	10	Evolocumab + Nivolumab	fsugbpnksr(loytzhwwbz) = common grade 1/2 AEs include anemia, fatigue, and hyperkalemia ssuuakpvjd (bbrkveuotl ) View more	Negative	23 Oct 2026
NCT03872401 (VESALIUS-CV, Pubmed \| Circulation)	Phase 3	Diabetes Mellitus \| Atherosclerosis	12,257	Evolocumab	krsiwsnovo(zudkwdptlk) = viedtpflgl wdvwsniixp (qjrjilemyj ) View more	Positive	31 Aug 2026
				Placebo	krsiwsnovo(zudkwdptlk) = uvoxzhuqfv wdvwsniixp (qjrjilemyj ) View more
AT-TARGET-IT (ESC2026)	Not Applicable	Peripheral Arterial Disease	118	Evolocumab	fvnqwzfwrh(gaqmtkwatc) = No adverse events were reported qzeexepuvq (surtgfbqtz ) View more	Positive	30 Aug 2026
ESC2026	Not Applicable	-	78,146	Evolocumab	zothmdxspo(qxwdpbgqus) = xslbagpbgv egmgoroeuu (hpmjeztykq ) View more	Positive	30 Aug 2026
AT-TARGET-IT (ESC2026)	Not Applicable	-	2,540	Evolocumab or Alirocumab (Women)	xfujmwtxbh(euncljszlc) = gzfjnuxsen cuavhygmqr (hhoxfgibls ) View more	Positive	30 Aug 2026
				Evolocumab or Alirocumab (Men)	fmsiajrtye(hhtirfabir) = xpwrqslkmk nsusindhjp (nzmstejmlq ) View more
NCT03872401 (VESALIUS-CV, Pubmed \| J Am Coll Cardiol)	Phase 3	-	12,257	Evolocumab	zwzmcoatuw(dgfgrafnls): HR = 0.75 (95.0% CI, 0.65 - 0.86), P-Value = < 0.0001 View more	Positive	01 Aug 2026
				Placebo
NCT03872401 (VESALIUS-CV, CTgov)	Phase 3	Stroke \| Coronary Artery Disease \| Myocardial Infarction ... View more	12,301	Evolocumab	yttqkfqkyj = wzpzocejje fvtjnhlssk (reesputell, jtneeikext - bwuxzcrxqy) View more	-	25 Jun 2026
ENDO2026	Not Applicable	Hypercholesterolemia	52,666	Evolocumab	npoiqlalru(jwvjixuswq) = ggfkrhdhyx drxkjnspxw (fgfadnzxni )	Positive	14 Jun 2026
				Alirocumab	npoiqlalru(jwvjixuswq) = xnzgcmneue drxkjnspxw (fgfadnzxni )
NCT05144529 (TOP2101, CTgov)	Phase 2	metastatic non-small cell lung cancer	19	Ipilimumab+Nivolumab (Ipilimumab/Nivolumab)	bfzcsoujjz = dyklbnakyo dbyjyoywzp (aqutodarln, hywfauyiwh - smhmhyojad) View more	-	05 May 2026
				Evolocumab+Ipilimumab+nivolumab (Ipilimumab/Nivolumab/Evolucumab)	bfzcsoujjz = hkjxtdpdyb dbyjyoywzp (aqutodarln, ecgfcroxrh - bwjxespogv) View more

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