Last update 24 Jun 2024

Alirocumab

Last update 24 Jun 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Monoclonal antibody

Synonyms

ALI, Alirocumab (USAN), Anti-PCSK9 monoclonal antibody(Regeneron/Sanofi)

+ [6]

Target

PCSK9

Mechanism

PCSK9 inhibitors(Proprotein convertase subtilisin kexin type 9 inhibitors)

Therapeutic Areas

Nervous System DiseasesCardiovascular DiseasesEndocrinology and Metabolic Disease+ [4]

Active Indication

Homozygous familial hypercholesterolemiaAngina, UnstableMyocardial Infarction+ [10]

Inactive Indication

Acute Coronary SyndromeHyperlipidemia Type IIaHyperlipoproteinemia Type II+ [1]

Originator Organization

Sanofi

Active Organization

Sanofi SA

Regeneron Pharmaceuticals, Inc.

Sanofi Winthrop Industrie SA

+ [3]

Inactive Organization

Sanofi-Aventis Recherche et Développement SA

Sanofi (China) Investment Co. Ltd.

Aventis Pharmaceuticals, Inc.

Drug Highest PhaseApproved

First Approval Date

US (24 Jul 2015),

AtherosclerosisHeterozygous familial hypercholesterolemiaHyperlipidemias

Regulation-

Gene Sequence

Sequence Code 175891L

Source: *****

Sequence Code 9724619H

Source: *****

118

Clinical Trials associated with Alirocumab

JPRN-UMIN000040727 / SuspendedPhase 4IIT

The crossover randomized controlled clinical trial with Alirocumab and Evolocumab:CROSS ALIVE Study - The crossover randomized controlled clinical trial with Alirocumab and Evolocumab:CROSS ALIVE Study

Start Date01 Jul 2025

Sponsor / Collaborator-

NCT06385262 / Not yet recruitingPhase 2IIT

Safety, Efficacy, and Tumor Immune Microenvironment Changes With Neoadjuvant Chemotherapy and Cemiplimab With or Without Alirocumab in Stage 1B-3A Non-Small Cell Lung Cancer: TOP 2301

In this open-label, two-arm, randomized phase 2 clinical trial, patients with clinical stage 1B-3A non-small cell lung cancer (NSCLC) will receive neoadjuvant chemotherapy and cemiplimab every 3 weeks for 3 cycles with or without alirocumab every 4 weeks prior to surgery.
Eligible patients will be randomized with equal allocation to two treatment groups. Permuted block randomization algorithm will be used for treatment assignment with stratification factors: stage (1B, 2A, 2B, 3A), and performance status (0 vs. 1).
The study hypothesis is that the addition of alirocumab to neoadjuvant chemoimmunotherapy will make tumor cells more immunogenic to cytotoxic T cells, resulting in an increase in complete pathologic responses in surgically resected tumor.

Start Date01 Jul 2024

Sponsor / Collaborator

Duke University

[+1]

ChiCTR2300078873 / RecruitingPhase 4IIT

The study of Alirocumab in the Treatment of Symptomatic Intracranial Atherosclerotic Plaques

Start Date01 Jan 2024

Sponsor / Collaborator-

100 Clinical Results associated with Alirocumab

100 Translational Medicine associated with Alirocumab

100 Patents (Medical) associated with Alirocumab

1,283

Literatures (Medical) associated with Alirocumab

01 Mar 2024·Metabolism: clinical and experimental

Inhibition of PCSK9 prevents and alleviates cholesterol gallstones through PPARα-mediated CYP7A1 activation

Article

Author: Ma, Xiaochen ; Chen, Zhenmei ; Li, Yitong ; Shao, Weiqing ; Zhang, Bo ; Zhang, Xiandi ; Yi, Chenhe ; Chen, Jinhong ; Ma, Yue ; Tao, Baorui ; Lin, Jing ; Geng, Yan ; Zhang, Rui

BACKGROUND & AIMS:

Dysregulated cholesterol metabolism is the major factor responsible for cholesterol gallstones (CGS). Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a critical role in cholesterol homeostasis and its inhibitors secure approval for treating various cholesterol metabolic disorders such as hypercholesterolemia and cardiovascular diseases, but its role in CGS remains unclear. Our study aims to clarify mechanisms by which PCSK9 promotes CGS formation and explore the application of the PCSK9 inhibitor, alirocumab, in preventing and treating CGS.

APPROACH & RESULTS:

The expressions of PCSK9 were notably increased in CGS patients' serum, bile, and liver tissues compared to those without gallstones. Moreover, among CGS patients, hepatic PCSK9 was positively correlated with hepatic cholesterol and negatively correlated with hepatic bile acids (BAs), suggesting PCSK9 was involved in disrupted hepatic cholesterol metabolism related to CGS. Mechanistically, in vitro experiments demonstrated that inhibition of PCSK9 enhanced nuclear expression of PPARα by diminishing its lysosomal degradation and subsequently activated CYP7A1 transcription. Finally, inhibition of PCSK9 prevented CGS formation and dissolved the existing stones in CGS mice by elevating the conversion of cholesterol into BAs through PPARα-mediated CYP7A1 activation. Additionally, serum PCSK9 level may function as a prognostic signature to evaluate the therapeutic efficacy of PCSK9 inhibitors.

CONCLUSIONS:

Inhibition of PCSK9 exerts preventive and therapeutic effects on CGS by activating PPARα-mediated CYP7A1 expression and facilitating the conversion of cholesterol into BAs, which highlights the potential of PCSK9 inhibition as a promising candidate for preventing and treating CGS in clinical applications.

IMPACT AND IMPLICATIONS:

PCSK9 plays a pivotal role in cholesterol metabolism and its inhibitors are approved for clinical use in cardiovascular diseases. Our study observes inhibition of PCSK9 prevents and dissolves CGS by activating PPARα-mediated CYP7A1 expression and facilitating the conversion of cholesterol into BAs. Mechanistically, PCSK9 inhibition enhanced the nuclear expression of PPARα by diminishing its lysosomal degradation and subsequently activated CYP7A1 transcription. Our study sheds light on the new function and mechanism of PCSK9 in CGS, providing a novel preventive and therapeutic target with potential clinical applications.

01 Mar 2024·Naunyn-Schmiedeberg's archives of pharmacology

Proprotein convertase subtilisin/kexin 9 inhibitor downregulates microRNA-130a-3p expression in hepatocytes to alleviates atherosclerosis progression

Article

Author: Han, Chuyi ; Li, Tingting ; Zuo, Junrong ; Jin, Dongxia ; Cong, Hongliang ; Zhao, Fumei ; Xu, Jinghan

Proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitors have been shown to regulate lipid metabolism and reduce the risk of cardiovascular events. This study explores the effect and potential mechanism of PCSK9 inhibitors on lipid metabolism and coronary atherosclerosis. HepG2 cells were incubated with PCSK9 inhibitor. ApoE-/- mice were fed with a high fat to construct an atherosclerosis model, and then treated with PCSK9 inhibitor (8 mg/kg for 8 w). PCSK9 inhibitor downregulated microRNA (miRNA)-130a-3p expression in a dose-dependent manner. And, miR-130a-3p could bind directly to the 3' untranslated region (3'-UTR) region of LDLR to down-regulate LDLR expression in HepG2 cells, as confirmed by the luciferase reporter gene assay. In addition, miR-130a-3p overexpression significantly attenuated the promoting effect of PCSK9 inhibitor on LDLR and DiI-LDL uptake in HepG2 cells. More importantly, in vivo experiments confirmed that PCSK9 inhibitor could significantly inhibit miR-130a-3p levels and promote LDLR expression in liver tissues, thus regulating serum lipid profile and alleviating the progression of coronary atherosclerosis. PCSK9 inhibitor could moderately improve coronary atherosclerosis by regulating miR-130a-3p/LDLR axis, providing an exploitable strategy for the treatment of coronary atherosclerosis.

09 Feb 2024·European heart journal. Acute cardiovascular care

Quality control to improve LDL-cholesterol management in patients with acute coronary syndromes based on the ACS EuroPath IV project

Article

Author: Catapano, Alberico L ; Jukema, J Wouter ; Schiele, François ; Zaman, Azfar ; Laufs, Ulrich ; De Caterina, Raffaele ; Sionis, Alessandro

Abstract:

Aims:

We performed quality control of lipid-lowering therapy (LLT) in patients with acute coronary syndrome (ACS), with a view to proposing corrective actions.

Methods and results:

Using a Define Measure Analysis Improve Control (DMAIC) approach applied to data from the ACS EuroPath IV survey, we measured attainment of two quality indicators (QIs) related to lipid-lowering treatment: (i) prescription of high-intensity statins (or equipotent treatment) before discharge, and (ii) proportion with LDL-cholesterol <55 mg/dL (1.4 mmol/L) during follow-up. A total of 530 European cardiologists responded and provided data for up to 5 patients from their centre, for acute and follow-up phases. Corrective measures are proposed to increase the rate of attainment of both QIs. Attainment of the first QI was measured in 929 acute-phase patients, 99% had LLT prescribed at discharge and 75% of patients fulfilled the first QI. Attainment of the second QI was assessed in 1721 patients with follow-up. The second QI was reached in 31% of patients. The DMAIC approach yielded 10 potential changes in prescription, 3 for the first and 7 for the second QI. The overall strategy is ‘Fire to Target’, i.e. early intensification of the LLT using statins, ezetimibe, bempedoic acid, and proprotein convertase subtilisin/kexin type-9 inhibitors, and is presented as an algorithm for routine application.

Conclusion:

Quality control for LLT, based on the ACS EuroPath IV survey, detected 10 potential changes in prescription that could enhance attainment of 2 QIs. Whether the Fire to Target strategy will be adopted and effective needs to be assessed in further steps of the EuroPath Quality programme.

159

News (Medical) associated with Alirocumab

11 Jun 2024

·pipelinereview.com

Kevzara® (sarilumab) Approved by FDA for the Treatment of Active Polyarticular Juvenile Idiopathic Arthritis (pJIA)

Approval in patients with pJIA weighing 63kg or greater adds to Kevzara’s position in treating adult chronic inflammatory conditions of moderately to severely active rheumatoid arthritis and polymyalgia rheumatica TARRYTOWN, NY and CAMBRIDGE, MA, USA I June 11, 2024 I Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) and Sanofi today announced that the U.S. Food and Drug Administration has approved Kevzara ® (sarilumab) for the treatment of patients weighing 63 kg or greater with active polyarticular juvenile idiopathic arthritis (pJIA), a form of arthritis that impacts multiple joints at a time. “Polyarticular juvenile idiopathic arthritis can be a painful disease for children where multiple joints are impacted by this chronic infammation,” said George D. Yancopoulos, M.D., Ph.D., Board co-Chair, President and Chief Scientific Officer at Regeneron. “Not only are their daily lives impacted, but their futures can be disrupted without adequate treatment. The approval of Kevzara in polyarticular juvenile idiopathic arthritis provides these vulnerable patients and their families a new FDA-approved treatment option to help navigate this disease.” The FDA approval in this patient population is supported by evidence from adequate and well-controlled studies and pharmacokinetic data from adults with rheumatoid arthritis as well as a pharmacokinetic, pharmacodynamic, dose finding and safety study in pediatric patients with pJIA. People living with pJIA may experience joint symptoms such as pain, stiffness and swelling, which may restrict their activities and make certain aspects of their day-to-day life incredibly challenging. The disease can lead to an increased risk of permanent joint damage as well as delayed growth and development, due to chronic joint inflammation. No new adverse reactions (ARs) and safety concerns were identified in the pJIA population compared to the rheumatoid arthritis population. The most common adverse drug reactions for patients with pJIA were nasopharyngitis, neutropenia, upper respiratory tract infection, and injection site erythema. The most common AR that resulted in permanent discontinuation of therapy with Kevzara was neutropenia. Overall, patients treated with Kevzara are at increased risk for developing serious infections that may lead to hospitalization or death. “This latest approval for Kevzara brings a new treatment option with an established efficacy and safety profile to pediatric patients living with polyarticular juvenile idiopathic arthritis,” said Brian Foard, Executive Vice President, Head, Specialty Care at Sanofi. “This milestone highlights our ongoing commitment to bringing medicines to our younger patients living with this chronic condition that can cause debilitating joint pain and inflammation.” Sanofi and Regeneron are committed to helping patients in the U.S. who are prescribed Kevzara gain access to the medicine and receive the support they may need. KevzaraConnect ® , a comprehensive and specialized program that provides support services to patients throughout every step of the treatment process, can help eligible patients who are uninsured, lack coverage, or need copay assistance. For more information, please call: 1-844-Kevzara (1-844-538-9272) or visit www.Kevzara.com . About Kevzara In addition to pJIA, Kevzara is currently approved in 25 countries to treat adults with moderately to severely active rheumatoid arthritis after at least one other medicine, called a disease modifying antirheumatic drug (DMARD), has been used and did not work well or could not be tolerated. Kevzara is also approved in the U.S. for the treatment of polymyalgia rheumatica – an inflammatory rheumatic disease – in adult patients who have had an inadequate response to corticosteroids or who cannot tolerate corticosteroid taper. Kevzara binds specifically to the IL-6 receptor and has been shown to inhibit IL-6-mediated signaling. IL-6 is an immune system protein produced in increased quantities in patients with rheumatoid arthritis and has been associated with disease activity, joint destruction and other systemic problems. Sarilumab is being jointly developed by Sanofi and Regeneron under a global collaboration agreement. About Regeneron’s VelocImmune ® Technology Regeneron’s VelocImmune technology utilizes a proprietary genetically engineered mouse platform endowed with a genetically humanized immune system to produce optimized fully human antibodies. When Regeneron’s co-Founder, President and Chief Scientific Officer George D. Yancopoulos was a graduate student with his mentor Frederick W. Alt in 1985, they were the first to envision making such a genetically humanized mouse, and Regeneron has spent decades inventing and developing VelocImmune and related VelociSuite ® technologies. Dr. Yancopoulos and his team have used VelocImmune technology to create a substantial proportion of all original, FDA-approved or authorized fully human monoclonal antibodies. This includes REGEN-COV ® (casirivimab and imdevimab), Dupixent ® (dupilumab), Libtayo ® (cemiplimab-rwlc), Praluent ® (alirocumab), Kevzara, Evkeeza ® (evinacumab-dgnb), Inmazeb ® (atoltivimab, maftivimab and odesivimab-ebgn) and Veopoz ® (pozelimab-bbfg). U.S. Indications and Important Safety Information KEVZARA ® (sarilumab) is an injectable prescription medicine called an interleukin-6 (IL-6) receptor blocker. KEVZARA is used to treat: Please click here to see full Prescribing Information including risk of SERIOUS SIDE EFFECTS and Medication Guide. About Regeneron Regeneron (NASDAQ: REGN) is a leading biotechnology company that invents, develops and commercializes life-transforming medicines for people with serious diseases. Founded and led for over 35 years by physician-scientists, our unique ability to repeatedly and consistently translate science into medicine has led to numerous FDA-approved treatments and product candidates in development, almost all of which were homegrown in our laboratories. Our medicines and pipeline are designed to help patients with eye diseases, allergic and inflammatory diseases, cancer, cardiovascular and metabolic diseases, hematologic conditions, infectious diseases and rare diseases. Regeneron is accelerating and improving the traditional drug development process through our proprietary VelociSuite ® technologies, such as VelocImmune, which uses unique genetically humanized mice to produce optimized fully human antibodies and bispecific antibodies, and through ambitious research initiatives such as the Regeneron Genetics Center ® , which is conducting one of the largest genetics sequencing efforts in the world. For more information, please visit www.Regeneron.com or follow Regeneron on LinkedIn . About Sanofi We are an innovative global healthcare company, driven by one purpose: we chase the miracles of science to improve people’s lives. Our team, across the world, is dedicated to transforming the practice of medicine by working to turn the impossible into the possible. We provide potentially life-changing treatment options and life-saving vaccine protection to millions of people globally, while putting sustainability and social responsibility at the center of our ambitions. SOURCE: Sanofi

Drug Approval

29 May 2024

·www.fiercebiotech.com

Chasing Merck, AstraZeneca's PCSK9 inhibitor lowers cholesterol in phase 1 test

AstraZeneca is significantly trailing Merck & Co. in the hypercholesterolaemia space. AstraZeneca’s small molecule lowered levels of “bad” cholesterol by more than half in patients who had never received treatment for their condition, according to results from an early-stage trial. The U.K. pharma presented the results today at the European Atherosclerosis Society in France, according to a release. AZD0780 is an oral small molecule PCSK9 inhibitor in development for dyslipidaemia, a condition characterized by elevated cholesterol in the blood that can progress to clogged arteries, also called atherosclerosis. The phase 1 trial is focused on this disease, however, an additional arm is testing the therapy in 35 patients with hypercholesterolaemia, or high cholesterol. High LDL-C, also known as "bad" cholesterol, is associated with a risk of cardiovascular disease. The main goal of the test was the safety, tolerability, pharmacokinetics and pharmacodynamics of AZD0780 in lowering LDL-C. In the hypercholesterolaemia arm presented at the conference, patients who took AZD0780 as well as a statin had a statistically significant 52% reduction in low-density lipoprotein cholesterol (LDL-C), with a 78% total reduction from baseline. The trial moved on to phase 2 in patients with dyslipidaemia earlier in the year, according to AstraZeneca. “AZD0780 inhibits PCSK9 via a novel, previously unexplored, mode of action that is compatible with traditional oral small molecule drug discovery,” said AstraZeneca’s Sharon Barr, executive vice president of biopharmaceuticals R&D, in a statement. “We are progressing development of AZD0780 as an innovative, convenient oral option for patients who are currently unable to meet their LDL-C targets with statins alone to reduce their risk of CV events.” AstraZeneca is significantly trailing Merck & Co. in the hypercholesterolaemia space. The rival’s oral PCSK9 inhibitor MK-0616 is already in three phase 3 trials to examine its ability to lower LDL-C and lower the risk of cardiovascular events. The primary completion date for the initial two studies in the trio is September 2025. The third trial is looking at cardiovascular outcomes and isn’t expected to wrap up until late 2029, after six years of watching patients. Both entrants are trying to replace Amgen’s Repatha and Sanofi-Regeneron’s Praluent, which are approved injectables for the same condition.

Clinical ResultPhase 2Phase 1Phase 3AHA

29 May 2024

·firstwordpharma.com

AstraZeneca’s cholesterol drug sets up oral PCSK9 showdown with Merck & Co.

AstraZeneca has taken the wraps off early data for its oral PCSK9 inhibitor AZD0780, setting the stage for a potential rivalry with Merck & Co.'s similar programme, dubbed MK-0616, as the two companies race to bring the first convenient pill form of these potent cholesterol-lowering drugs to market. Findings were presented Wednesday at the annual meeting of the European Atherosclerosis Society (EAS).The Phase I study evaluated two dose levels of AZD0780, 30mg and 60mg, administered orally once daily for 28 days to separate cohorts of 15 participants each, compared to a placebo group of equal size. Separately, 35 participants with LDL levels ranging from 100 to 190mg/dL took the statin Crestor (rosuvastatin) for 3 weeks, followed by either 30mg of AZD0780 or placebo for another 4 weeks.Over 50% decline in 'bad' cholesterolResults demonstrated that AZD0780, when administered to treatment-naive hypercholesterolaemic patients after the Crestor run-in period, achieved a statistically significant 52% reduction in LDL cholesterol versus Crestor alone. The total reduction in LDL was 78% when compared to baseline levels.As monotherapy, the low and high AZD0780 doses cut cholesterol levels by 30% and 38%, respectively, versus baseline. Preliminary data also suggested that food increased total exposure by about 30% compared to fasting. No serious adverse events were reported.Advantages over current injectablesRegina Fritsche Danielson, global head of research and early development, cardiovascular, renal and metabolic diseases at AstraZeneca, underscored the advantages an effective oral PCSK9 option could hold over currently marketed monoclonal antibodies like Sanofi and Regeneron Pharmaceuticals' Praluent (alirocumab) and Amgen's Repatha (evolocumab), which are both injected."Many patients are not really open to take an injectable, and physicians are not so keen to prescribe the injectable PCSK9, so now we have an alternative and simple small tablet that we can give to these patients to really control the LDL cholesterol," Danielson told FirstWord. Achieving 50% more cholesterol lowering on top of statins could enable over 90% of patients to hit target cholesterol levels, she says, a key goal given the cardiovascular (CV) risk that persists in many people despite existing therapies.Merck's contenderWhile Merck's MK-0616 generated excitement earlier by posting around 60% LDL-cholesterol reductions at the highest dose in Phase II testing, analysts at Jefferies suggest AstraZeneca's design could prove advantageous. Unlike Merck's macrocyclic peptide, which requires a GI absorption enhancer, "AZD0780 is a true small molecule, from a prior acquisition of Dogma Therapeutics, and so should not have meaningful food effects," they said.Merck kicked off a Phase III programme for MK-0616 last year. In addition to a pair of registrational studies to evaluate LDL-cholesterol reduction, the company launched a Phase III CV outcomes study last October, with a planned 2029 readout. See – Spotlight On: Merck & Co.'s oral PCSK9 - why it's so important.The AZD0780 data come as AstraZeneca has laid out an ambitious plan to nearly double its revenues to $80 billion by 2030. During the company's recent investor day, management hinted that AZD0780 could also be part of a combination with its next-generation oral GLP-1 agonist AZD5004. For more, see Spotlight On: AstraZeneca's bold ambitions - the key takeaways.Phase II data by year-endBut for now, the focus for AZD0780 is on curbing LDL cholesterol. AstraZeneca started a Phase II dyslipidaemia study in January that is "recruiting extremely well," according to Danielson, "so we actually are very hopeful that we will have the data towards the end of this year." The company is anticipating an end-of-Phase-II meeting when the study wraps up to discuss the Phase III design. Danielson did not want to tease any timelines for when AZD0780 could hit the market, but said that "it's a very accelerated programme."

Clinical ResultPhase 2Phase 1Phase 3

100 Deals associated with Alirocumab

External Link

KEGG	Wiki	ATC	Drug Bank
D10335	Alirocumab	C10AX14	DB09302

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Homozygous familial hypercholesterolemia	US	Regeneron Pharmaceuticals, Inc.	01 Apr 2021
Angina, Unstable	US	Regeneron Pharmaceuticals, Inc.	26 Apr 2019
Myocardial Infarction	US	Regeneron Pharmaceuticals, Inc.	26 Apr 2019
Stroke	US	Regeneron Pharmaceuticals, Inc.	26 Apr 2019
Primary Hyperlipidemia	CA	Sanofi	29 Apr 2016
Hypercholesterolemia	CH	Sanofi	22 Apr 2016
Dyslipidemias	EU	Sanofi Winthrop Industrie SA	23 Sep 2015
Dyslipidemias	IS	Sanofi Winthrop Industrie SA	23 Sep 2015
Dyslipidemias	LI	Sanofi Winthrop Industrie SA	23 Sep 2015
Dyslipidemias	NO	Sanofi Winthrop Industrie SA	23 Sep 2015
Primary hypercholesterolemia	EU	Sanofi Winthrop Industrie SA	23 Sep 2015
Primary hypercholesterolemia	IS	Sanofi Winthrop Industrie SA	23 Sep 2015
Primary hypercholesterolemia	LI	Sanofi Winthrop Industrie SA	23 Sep 2015
Primary hypercholesterolemia	NO	Sanofi Winthrop Industrie SA	23 Sep 2015
Atherosclerosis	US	Regeneron Pharmaceuticals, Inc.	24 Jul 2015
Heterozygous familial hypercholesterolemia	US	Regeneron Pharmaceuticals, Inc.	24 Jul 2015
Hyperlipidemias	US	Regeneron Pharmaceuticals, Inc.	24 Jul 2015

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Acute Coronary Syndrome	Phase 3	US	Sanofi (China) Investment Co. Ltd.	11 Oct 2012
Acute Coronary Syndrome	Phase 3	US	Sanofi-Aventis Recherche et Développement SA	11 Oct 2012
Acute Coronary Syndrome	Phase 3	JP	Sanofi (China) Investment Co. Ltd.	11 Oct 2012
Acute Coronary Syndrome	Phase 3	JP	Sanofi-Aventis Recherche et Développement SA	11 Oct 2012
Acute Coronary Syndrome	Phase 3	AR	Sanofi-Aventis Recherche et Développement SA	11 Oct 2012
Acute Coronary Syndrome	Phase 3	AR	Sanofi (China) Investment Co. Ltd.	11 Oct 2012
Acute Coronary Syndrome	Phase 3	BE	Sanofi-Aventis Recherche et Développement SA	11 Oct 2012
Acute Coronary Syndrome	Phase 3	BE	Sanofi (China) Investment Co. Ltd.	11 Oct 2012
Acute Coronary Syndrome	Phase 3	BA	Sanofi-Aventis Recherche et Développement SA	11 Oct 2012
Acute Coronary Syndrome	Phase 3	BA	Sanofi (China) Investment Co. Ltd.	11 Oct 2012

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


PACMAN (ESC2023)	Not Applicable	Acute myocardial infarction	300	Alirocumab	kbivrbzatx(enmaonrkil) = eayppwuyfn hgvakyqcxq (qfdwscomer ) View more	Positive	28 Aug 2023
				Placebo	kbivrbzatx(enmaonrkil) = vverwwsqsl hgvakyqcxq (qfdwscomer ) View more
ODYSSEY OUTCOMES (ESC2023)	Not Applicable	Lp(a)	-	Alirocumab	pdrmdngvlz(hsxpyjodxl): RR = 0.83 (95% CI, 0.74 - 0.92)	-	26 Aug 2023
				Placebo
NCT03067844 (PACMAN-AMI, Pubmed)	Phase 3	Acute myocardial infarction	300	Alirocumab	wsrleocpbf(dsbwvaymxb): odds ratio = 1.7 (95% CI, 0.9 - 3.0), P-Value = 0.076 View more	-	21 Jun 2023
				Placebo
NCT01663402 (ODYSSEY OUTCOMES, Pubmed)	Phase 3	Acute Coronary Syndrome	18,924	Alirocumab	xvmtonnpdw(cawovykgsn) = izqlnaqhqi sfjsnzfgxx (vnnvjguizg )	-	16 Jun 2023
				Placebo	xvmtonnpdw(cawovykgsn) = lrysbfeaje sfjsnzfgxx (vnnvjguizg )
NCT01663402 (ODYSSEY OUTCOMES, Pubmed)	Phase 3	Acute Coronary Syndrome	18,924	Alirocumab	xidqberfxz(pxcktuprud) = cugbsxrbzj sedxlzpvuk (umqakzxeel ) View more	-	26 Apr 2023
				Placebo	xidqberfxz(pxcktuprud) = neecycuntl sedxlzpvuk (umqakzxeel ) View more
NCT05465278 (ARCHITECT, Pubmed)	Phase 4	Coronary Artery Disease	104	Alirocumab	ghbzgohzsx(yctnmmieut) = hzsbftvxde fxnkobzecy (yshnpwrujs ) View more	-	03 Apr 2023
NCT03510715 (Pubmed)	Phase 3	Homozygous familial hypercholesterolemia	18	Alirocumab 75 mg	cnlrwzfbtc(ghzqfnefhh) = hqexjfhpur mcethxlbwa (mnuosfksje )	Positive	03 Nov 2022
NCT01663402 (ODYSSEY OUTCOMES, Pubmed)	Phase 3	Acute Coronary Syndrome apolipoprotein B	-	Alirocumab	qbfhurgpbn(fpzcnjuasd) = pebxbdhjhi qbghotujeh (dwctevzqsf, 3.78 - 4.79)	Positive	30 Aug 2022
				Placebo	qbfhurgpbn(fpzcnjuasd) = inrtyxvoqr qbghotujeh (dwctevzqsf, 2.9 - 3.6)
NCT03067844 (PACMAN-AMI, ESC2022) Manual	Phase 3	Acute myocardial infarction	139	Alirocumab	buhmkurqig(wlxidhprzg) = cgurjtutcr acbdqkggtm (vgjfjrynyv, 2.24) View more	Negative	29 Aug 2022
				Placebo	buhmkurqig(wlxidhprzg) = idwguizyyw acbdqkggtm (vgjfjrynyv, 2.19) View more
PACMAN-AMI (ESC2022)	Not Applicable	Acute myocardial infarction PCSK9	139	Alirocumab	ehgowbdjli(zzmeotcimh) = kjtlcpxtum csnsfgrpum (qhkkujbplv ) View more	Negative	29 Aug 2022
				Placebo	ehgowbdjli(zzmeotcimh) = yxtqzcwyrw csnsfgrpum (qhkkujbplv ) View more

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Leverages most recent intelligence information, enabling fullest potential.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis