Around the world, about 4 in 10 adults have abnormal blood fat levels-known as dyslipidaemia-which raises their chances of getting heart disease. Many people with this condition are prescribed statins, medications that help lower the "bad" Low-density lipoprotein cholesterol (LDL-C) in the blood and, in doing so, help prevent serious heart-related problems. While statins do lower these harmful cholesterol levels, recent research suggests that statins might interfere with some of the positive effects that exercise typically has on muscle cells' energy centers (the mitochondria) and on a person's aerobic capacity. It is not yet fully understood how statins might influence these exercise benefits at the molecular level. To address this gap, the present study will look closely at how taking statins combined with a structured exercise program affects both the muscle cells and the whole-body fitness of people with dyslipidaemia. By using a wide-ranging protein analysis, the research aims to identify changes in muscle proteins and other metabolism-related factors that could explain why statins might alter the expected improvements from exercise.
Methods and Analysis In this 12-week study, 100 adults between the ages of 40 and 65 who have dyslipidaemia but no established heart disease will take part. Participants will be randomly split into one of four groups: (1) exercise plus a placebo (an inactive pill), (2) exercise plus a daily high-dose statin (atorvastatin, 80 mg), (3) a daily high-dose statin without exercise, or (4) a placebo without exercise. More participants will be placed in the exercise groups to better understand the combined effects of exercise and statins. The main measurement will be how well the muscle's mitochondria work, assessed by changes in an enzyme called citrate synthase (CS) from before the program to after. Other important measures will include overall fitness (using a peak oxygen uptake (VO2peak) test) and detailed protein analyses. The study will also look at genetic variations to see if they influence how each participant responds to the treatment.
Ethics and Sharing of Results The study has received approval from the Faroe Islands Ethical Committee (2024-10) and follows international guidelines to protect participants' rights and data. Once the research is complete, the findings will be shared in leading scientific journals for the broader public and medical community to learn from.

Start Date01 May 2025

Sponsor / Collaborator

University of the Faroe Islands

[+1]

NCT06632379

/ Not yet recruitingPhase 4IIT

AtorvaStatin Postpartum and Reduction of Cardiovascular risK (SPARK): A Randomized Placebo-controlled Trial of Atorvastatin Postpartum for Reduction of Cardiovascular Risk

The objective is to conduct a double-blinded randomized controlled trial of atorvastatin vs. placebo among postpartum individuals with hypertensive disorders of pregnancy, to improve cardiovascular risk score postpartum. For this, 76 individuals with hypertensive disorders of pregnancy (HDP) will be randomized to atorvastatin 10mg or placebo, which will be started in the postpartum period after cessation of breast feeding and continued for 3 months.

Start Date15 Feb 2025

Sponsor / Collaborator

The Ohio State University

NCT06789432

/ Not yet recruitingPhase 4

Efficacy and Safety of Atorvastatin and Ezetimibe (10/10mg) Fixed Dose Combination Versus Atorvastatin (20mg) Monotherapy in Bangladeshi Population

The goal of this clinical trial is to evaluate the efficacy and safety of a fixed-dose combination of atorvastatin (10 mg) and ezetimibe (10 mg) compared to atorvastatin (20 mg) monotherapy in the Bangladeshi population.
Researchers will compare atorvastatin (10 mg) and ezetimibe (10 mg) to atorvastatin (20 mg) monotherapy to see if atorvastatin (10 mg) and ezetimibe (10 mg) FDC works to treat dyslipidemia.
Participants will:
* Take a fixed-dose combination of atorvastatin (10 mg) and ezetimibe (10 mg) compared to atorvastatin (20 mg) monotherapy for 3 months
* Follow-up visits at 6 weeks and 12 weeks for checkups and tests

Start Date01 Feb 2025

Sponsor / Collaborator

Beximco Pharmaceuticals Ltd.

100 Clinical Results associated with Atorvastatin Calcium

100 Translational Medicine associated with Atorvastatin Calcium

100 Patents (Medical) associated with Atorvastatin Calcium

14,126

Literatures (Medical) associated with Atorvastatin Calcium

01 Apr 2025·SEPARATION AND PURIFICATION TECHNOLOGY

Using artificial neural networks to elucidate retention interactions on stationary phases with amine moieties dedicated to supercritical fluid chromatography

Author: Plachka, Katerina ; Gazarkova, Tatana ; Pilarova, Veronika ; Plachká, Kateřina ; Nováková, Lucie ; Pilařová, Veronika ; Svec, Frantisek ; Švec, František ; Garrigues, Jean-Christophe ; Novakova, Lucie ; Gazárková, Taťána

The retention mechanisms of small mols. on a wide range of stationary phases using different mobile phase compositions are one of the most discussed topics in current state-of-the-art supercritical fluid chromatog. (SFC).Although various theories have been published on retention behavior, prediction, and stability over time, an in-depth insight into the mechanisms is still lacking.Our study focused on the description of the retention mechanisms on columns with amine moieties, i.e., 2-ethylpyridine, 2-picolylamine, 1-aminoanthracene, and diethylamine, dedicated to SFC, using three different compositions of organic modifier, i.e., methanol, methanol + 10 mmol/L NH₃, and methanol + 2% H₂O, in CO₂.An extensive set of analytes characterized by more than 200 mol. descriptors was used.The importance of the effect of each mol. descriptor on the retention behavior was determined by artificial neural networks.Thus, the descriptors increasing and/or decreasing retention on individual columns using different mobile phase compositions were defined.The data collected over one year of column use were statistically evaluated to describe the retention behavior of small mols. on the tested stationary phases using three organic modifiers and to describe the changes in retention behavior over time.As the development of the SFC method can be laborious and time-consuming, this publication offers a detailed description of the interactions taking place between the analyte and the SFC stationary phase.Understanding these fundamental processes will enable faster development of SFC methods using quality-by-design principles.

01 Feb 2025·CLINICAL PHARMACOLOGY & THERAPEUTICS

Risk of Opioid Overdose Associated with Concomitant Use of Methadone and Statins

Article

Author: Bilker, Warren B. ; Hennessy, Sean ; Brensinger, Colleen M. ; Miano, Todd A. ; Chen, Cheng ; Leonard, Charles E.

Methadone has a high potential for risky drug–drug interactions that can lead to opioid overdose, yet evidence on the magnitude of this risk remains limited. Since methadone is transported via P‐glycoprotein (P‐gp), the use of statins that inhibit P‐gp may elevate methadone plasma concentrations, potentially leading to opioid overdose. We explored this hypothesis by examining whether concomitant use of methadone and P‐gp‐inhibiting statins was associated with opioid overdose. Using Medicaid claims data from 2003 to 2020, we conducted a cohort study among new concomitant users of methadone and statins. We compared overdose rates among individuals exposed to P‐gp‐inhibiting statins (simvastatin, atorvastatin, or lovastatin) vs. those exposed to rosuvastatin (negative control), adjusting for baseline covariates. We identified 69,263 individuals newly exposed to methadone and a statin of interest; the overall incidence rate of opioid overdose was 26.0 per 1,000 person‐years. Adjusted hazard ratios (HRs) for methadone + P‐gp‐inhibiting statins consistently showed no association, ranging from 0.76 (95% CI = 0.48–1.22) for atorvastatin to 0.78 (95% CI = 0.50–1.22) for simvastatin, compared with methadone + rosuvastatin. Similar results were observed in sensitivity analysis that treated all P‐gp‐inhibiting statins as a single exposure group, as well as analyses stratified by baseline diagnosis of opioid use disorder or overdose, the duration of baseline methadone use, and calendar year intervals. Our findings suggest that concomitant use of methadone with simvastatin, atorvastatin, or lovastatin is not associated with the risk of opioid overdose compared to concomitant use of methadone and rosuvastatin.

01 Feb 2025·Biochemical genetics

Role of C/EBP Homologous Protein in Vascular Stenosis After Carotid Artery Injury

Article

Author: Cao, Cun-Yu ; Zhou, Fei ; Ding, Jia-Wang ; Zhou, Zi-Yi ; Teng, Lin ; He, Chao ; Qin, Qin ; Yang, Jian

The study aims to explore the fluctuating expression of C/EBP Homologous Protein (CHOP) following rat carotid artery injury and its central role in vascular stenosis. Using in vivo rat carotid artery injury models and in vitro ischemia and hypoxia cell models employing human aortic endothelial cells (HAECs) and vascular smooth muscle cells (T/G HA-VSMCs), a comprehensive investigative framework was established. Histological analysis confirmed intimal hyperplasia in rat models. CHOP expression in vascular tissues was assessed using Western blot and immunohistochemical staining, and its presence in HAECs and T/G HA-VSMCs was determined through RT-PCR and Western blot. The study evaluated HAEC apoptosis, inflammatory cytokine secretion, cell proliferation, and T/G HA-VSMCs migration through Western blot, ELISA, CCK8, and Transwell migration assays. The rat carotid artery injury model revealed substantial fibrous plaque formation and vascular stenosis, resulting in an increased intimal area and plaque-to-lumen area ratio. Notably, CHOP is markedly elevated in vessels of the carotid artery injury model compared to normal vessels. Atorvastatin effectively mitigated vascular stenosis and suppresses CHOP protein expression. In HAECs, ischemia and hypoxia-induced CHOP upregulation, along with heightened TNFα, IL-6, caspase3, and caspase8 levels, while reducing cell proliferation. Atorvastatin demonstrated a dose-dependent suppression of CHOP expression in HAECs. Downregulation of CHOP or atorvastatin treatment led to reduced IL-6 and TNFα secretion, coupled with augmented cell proliferation. Similarly, ischemia and hypoxia conditions increased CHOP expression in T/G HA-VSMCs, which was concentration-dependently inhibited by atorvastatin. Furthermore, significantly increased MMP-9 and MMP-2 concentrations in the cell culture supernatant correlated with enhanced T/G HA-VSMCs migration. However, interventions targeting CHOP downregulation and atorvastatin usage curtailed MMP-9 and MMP-2 secretion and suppressed cell migration. In conclusion, CHOP plays a crucial role in endothelial injury, proliferation, and VSMCs migration during carotid artery injury, serving as a pivotal regulator in post-injury fibrous plaque formation and vascular remodeling. Statins emerge as protectors of endothelial cells, restraining VSMCs migration by modulating CHOP expression.

News (Medical) associated with Atorvastatin Calcium

29 Jan 2025

·www.prnewswire.com

Tyra Biosciences Announces Appointment of Adele Gulfo to Board of Directors

CARLSBAD, Calif., Jan. 29, 2025 /PRNewswire/ -- Tyra Biosciences, Inc. (Nasdaq: TYRA), a clinical-stage biotechnology company focused on developing next-generation precision medicines that target large opportunities in Fibroblast Growth Factor Receptor (FGFR) biology, announced today the appointment of Adele Gulfo to its Board of Directors. Ms. Gulfo brings nearly three decades of executive leadership experience to the TYRA board, with a strong track record in developing and commercializing some of the world's best-selling medicines at Pfizer, AstraZeneca, Viatris and Sumitomo Pharma. "Adele is one of the most accomplished drug developers in our industry, with nearly thirty years of global expertise in product commercialization. She has been instrumental in the development and approval of multiple drugs across several therapeutic areas, including blockbuster medicines like LIPITOR® and CRESTOR®," said Todd Harris, CEO of TYRA. "Adele has a diversified background both as a pharmaceutical executive and board member, with a wealth of knowledge in growing oncology business units. Her experience in launching ORGOVYX® for prostate cancer will be particularly valuable as we plan for late-stage development of TYRA-300 in non-muscle invasive bladder cancer. We look forward to Adele's insights as we advance our precision medicine pipeline and continue to grow TYRA." Most recently, Ms. Gulfo served as Chief Executive Officer, Biopharma Commercial Unit, for Sumitomo Pharma America, Inc. where she led the commercial and development portfolio for multiple therapeutic areas including oncology, rare disease, urology, CNS and Women's Health. Previously, Ms. Gulfo served as chief commercial and business development officer at Sumitovant Biopharma from 2020 to 2023. Previously, she served as chief commercial development officer at Roivant Sciences, where she was influential in the formation of Sumitovant and in preparations for the launches of key brands, including ORGOVYX® (prostate cancer), GEMTESA (overactive bladder), RETHYMIC (congenital athymia), and MYFEMBREE (women's health). Adele was the president and general manager of Pfizer's $12B+ U.S. primary care business unit, as well as country manager for Pfizer's U.S. Biopharma business, including specialty and oncology business units. Earlier in her career at Pfizer, Adele was instrumental in the development, launch, and commercial success of LIPITOR®, which became the world's best-selling medicine. Prior to Pfizer, Adele held vice president roles within AstraZeneca, including business development and innovation and commercial readiness, as well as the multi-billion-dollar cardiovascular business unit. She oversaw the launch of Crestor® and its growth into a $2 billion medicine. Ms. Gulfo received a BS in biology from Seton Hall University and an MBA in marketing with highest honors from Fairleigh Dickinson University. She studied post-graduate molecular biology at the University of Medicine and Dentistry of New Jersey where she began her career. Ms. Gulfo has been awarded several patents over her career and has extensive public company board experience. Currently, Ms. Gulfo serves on the board of directors of Enpro, a publicly traded industrial engineering firm, and the Innovation Growth Board for Mass General Brigham, the largest hospital-based research enterprise in the United States. "TYRA has great potential to develop best-in-class precision medicines in therapeutic areas like non-muscle invasive bladder cancer and skeletal dysplasia, which represent large market opportunities where innovation is desperately needed," said Ms. Gulfo. "I look forward to partnering with the executive leadership team and other members of the board and leveraging my experience to advance and grow TYRA's pipeline." About Tyra Biosciences Tyra Biosciences, Inc. (Nasdaq: TYRA) is a clinical-stage biotechnology company focused on developing next-generation precision medicines that target large opportunities in FGFR biology. The Company's in-house precision medicine platform, SNÅP, enables rapid and precise drug design through iterative molecular SNÅPshots that help predict genetic alterations most likely to cause acquired resistance to existing therapies. TYRA's expertise in FGFR biology has created a differentiated pipeline with three clinical-stage programs in targeted oncology and genetically defined conditions. The Company's lead precision medicine stemming from SNÅP, TYRA-300, is a potential first-in-class selective FGFR3 inhibitor that is designed to avoid the toxicities associated with inhibition of FGFR1, FGFR2 and FGFR4, while being agnostic for the FGFR3 gatekeeper mutations. TYRA-300 is expected to be evaluated in three Phase 2 studies: SURF302 for IR NMIBC, BEACH301 for pediatric achondroplasia and SURF301 for metastatic urothelial cancer. TYRA is also developing TYRA-200, an oral, investigational, FGFR1/2/3 inhibitor, in the SURF201 study for metastatic intrahepatic cholangiocarcinoma, and TYRA-430, an oral, investigational FGFR4/3-biased inhibitor for FGF19+/FGFR4-driven cancers. TYRA is based in Carlsbad, CA. For more information about our science, pipeline and people, please visit and engage with us on LinkedIn. Forward-Looking Statements TYRA cautions you that statements contained in this press release regarding matters that are not historical facts are forward-looking statements. The forward-looking statements are based on our current beliefs and expectations and include, but are not limited to: the expected advancement of our pipeline and our growth; the potential to develop next-generation precision medicines and their potential to be first-in-class and/or best-in-class; the potential safety and therapeutic benefits of, and market opportunities for, our product candidates; the expected timing and phase of development of TYRA-300; and the potential for SNÅP to develop therapies. Actual results may differ from those set forth in this press release due to the risks and uncertainties inherent in our business, including, without limitation: later developments with the FDA may be inconsistent with prior feedback from the FDA; we are early in our development efforts, have only recently begun testing TYRA-300 and TYRA-200 for oncology in clinical trials and the approach we are taking to discover and develop drugs based on our SNÅP platform is novel and unproven and it may never lead to product candidates that are successful in clinical development or approved products of commercial value; potential delays in the commencement, enrollment, data readouts and completion of preclinical studies and clinical trials; results from preclinical studies or early clinical trials not necessarily being predictive of future results; interim results of a clinical trial are not necessarily indicative of final results and one or more of the clinical outcomes may materially change as patient enrollment continues, following more comprehensive reviews of the data, as follow-up on the outcome of any particular patient continues and as more patient data becomes available, including the risk that unconfirmed responses may not ultimately result in confirmed responses to treatment after follow-up evaluations; unexpected adverse side effects or inadequate efficacy of our product candidates that may limit their development, regulatory approval, and/or commercialization; the potential for our programs and prospects to be negatively impacted by developments relating to our competitors, including the results of studies or regulatory determinations relating to our competitors; and other risks described in our prior filings with the Securities and Exchange Commission (SEC), including under the heading "Risk Factors" in our annual report on Form 10-K and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and we undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Contact: Amy Conrad [email protected] SOURCE Tyra Biosciences WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Executive ChangePhase 2

23 Dec 2024

·endpts.com

Viatris' India-based manufacturing site blocked from shipping 11 generic drugs to US

Generic drug firm Viatris announced Monday that one of its India-based manufacturing facilities has been placed on import alert by the FDA following receipt of a warning letter for deficiencies cited from an inspection earlier this year. The company said 11 of its generic drugs will be barred from entering the US until the warning letter for the Indore, India-based site can be lifted. The company did not respond to a request for comment on which drugs have been halted entry to the US. However, due to drug shortages in the US, the FDA said four generic drugs made at the site are excluded from the import block, including levothyroxine sodium tablets, fingolimod capsules, atorvastatin tablets and metformin tablets. “Following the substance of FDA’s original inspection observations, we immediately implemented a comprehensive remediation plan at the site,” Viatris said in a statement on Monday. “The necessary corrective and preventive actions are well underway, including but not limited to related personnel actions. Additionally, we have engaged independent third-party subject matter experts to support the remediation plan.” The warning letter has yet to be released publicly. The company said the import alert does not affect its 2024 financial guidance, and it will incorporate potential future financial impact in its 2025 guidance early next year.

11 Dec 2024

·www.echemi.com

Heng Rui Pharma Launches Phase III Trial for ANGPTL3 Monoclonal Antibody

According to information from the U.S. clinical trial registry Clinicaltrials on December 10, Chinese company Heng Rui Pharma has launched its first Phase III clinical trial (SHR-1918-301) for the ANGPTL3 monoclonal antibody SHR-1918. This drug marks the first domestic ANGPTL3 monoclonal antibody to enter the Phase III clinical trial stage. SHR-1918 is an ANGPTL3 monoclonal antibody developed by Heng Rui Pharma, which works by inhibiting ANGPTL3 activity to lower triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) levels in serum. LDL-C and TG are significant risk factors for the development of atherosclerotic cardiovascular diseases. ANGPTL3 plays a key role in lipid metabolism regulation by inhibiting lipoprotein lipase and endothelial lipase, thereby reducing the clearance of TG and LDL-C. In September this year, Heng Rui Pharma announced the results of its first Phase I study (SHR-1918-101) at the European Society of Cardiology (ESC) annual meeting. The study showed that SHR-1918 (100-1200mg, subcutaneously) demonstrated good tolerance and pharmacokinetic characteristics in healthy subjects, with a peak time of 8.0-10.0 days and a half-life of 29.4-53.5 days. Additionally, SHR-1918 effectively and durably reduced LDL-C and TG levels: patients receiving doses of SHR-1918 of 300mg or higher had LDL-C levels reduced by over 30% (up to 49.1%), lasting more than 64 days; TG levels were reduced by over 50% (up to 82.8%), lasting more than 85 days. Given the potential of SHR-1918 for treating rare dyslipidemia disorders, the drug received breakthrough therapy designation for homozygous familial hypercholesterolemia (HoFH) from the Chinese National Medical Products Administration (NMPA) in September. The launched Phase III study is a multicenter, randomized, double-blind, placebo-controlled clinical trial (n=45), aimed at evaluating the efficacy and safety of SHR-1918 in treating homozygous familial hypercholesterolemia (HoFH). The primary endpoint is the percentage change in LDL-C levels from baseline at week 12. Homozygous familial hypercholesterolemia (HoFH) is a rare and severe genetic disorder where patients accumulate LDL-C in the blood due to defects or deficiencies in low-density lipoprotein receptors (LDLR), increasing the risk of heart disease and stroke. Currently, available treatment options for these patients include statins (simvastatin, atorvastatin, and rosuvastatin), ezetimibe, lomitapide, mipomersen, PCSK9 monoclonal antibodies (evolocumab and alirocumab), and evinacumab. Among these, evinacumab (Regeneron/Ultragenyx) is the only marketed ANGPTL3 monoclonal antibody, with global sales of $80.9 million in 2023.

Phase 3Clinical ResultPhase 1Breakthrough TherapyPhase 2

100 Deals associated with Atorvastatin Calcium

External Link

KEGG	Wiki	ATC	Drug Bank
D02258	Atorvastatin Calcium	C10AA05	DBSALT000011

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Heart Failure	US	Upjohn Manufacturing Ireland Unlimited Co.	02 Mar 2007
Angina Pectoris	US	Upjohn Manufacturing Ireland Unlimited Co.	21 Sep 2005
Myocardial Infarction	US	Upjohn Manufacturing Ireland Unlimited Co.	21 Sep 2005
Stroke	US	Upjohn Manufacturing Ireland Unlimited Co.	21 Sep 2005
Heterozygous familial hypercholesterolemia	US	Upjohn Manufacturing Ireland Unlimited Co.	18 Oct 2002
Hyperlipoproteinemia Type II	JP	Pfizer Inc.	10 Mar 2000
Hyperlipoproteinemia Type II	JP	Astellas Pharma, Inc.	10 Mar 2000
Hyperlipoproteinemia Type II	JP	Viatris Pharmaceutical GK	10 Mar 2000
Coronary Disease	CN	Beijing Jialin Pharmaceutical Co., Ltd.	01 Jan 1999
Hypercholesterolemia	AU	Aspen Pharmacare Australia Pty Ltd.	25 Sep 1997
Hypertension	AU	Aspen Pharmacare Australia Pty Ltd.	25 Sep 1997
Homozygous familial hypercholesterolemia	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996
Hyperlipidemia Type IIa	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996
Hyperlipoproteinemia Type IIb	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996
Hyperlipoproteinemia Type III	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996
Hyperlipoproteinemia Type IV	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996
Primary hypercholesterolemia	US	Upjohn Manufacturing Ireland Unlimited Co.	17 Dec 1996

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Acquired Immunodeficiency Syndrome	Phase 3	TH	Pfizer Inc.	01 Jan 2014
Immune Reconstitution Inflammatory Syndrome	Phase 3	TH	Pfizer Inc.	01 Jan 2014
Tuberculosis	Phase 3	TH	Pfizer Inc.	01 Jan 2014
Retinal Vein Occlusion	Phase 3	CA	Pfizer Inc.	01 Aug 2007
Systemic Lupus Erythematosus	Phase 3	TW	Pfizer Inc.	01 Mar 2007
Hypertriglyceridemia	Phase 3	-	GSK Plc	01 Feb 2007
Carotid Stenosis	Phase 3	US	Viatris, Inc.	01 Jan 2007
Atherosclerosis	Phase 3	TR	Pfizer Inc.	01 Nov 2006
Dyslipidemias	Phase 3	TR	Pfizer Inc.	01 Nov 2006
Vascular Calcification	Phase 3	TR	Pfizer Inc.	01 Nov 2006

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03351998 (CTgov)	Phase 4	Mitochondrial Diseases	68	Placebo Oral Tablet (Placebo)	rcvevzfwcr(wbutxixbhe) = ytvwdntjwo ykidjvqrgu (uuqhdnobua, yukpywzqvd - nndvbxodob) View more	-	18 Dec 2024
				Lipitor 20Mg Tablet (Low Dose Statin)	rcvevzfwcr(wbutxixbhe) = phnskendcx ykidjvqrgu (uuqhdnobua, fqlhxwmxet - selcypxusz) View more
NCT02740699 (CTgov)	Phase 4	Cardiovascular Diseases	79	Cardiac Magnetic Resonance Image (MRI)+Atorvastatin+Rosuvastatin	tjwyiplpaa(guodmpwmqu) = rgitaeyrsq rkpcadqblh (crfpjprjbj, qxwiedrrwd - sebqdqrmgt) View more	-	09 Oct 2024
NCT03872388 (CTgov)	Phase 2	Inflammatory Breast Neoplasms \| Triple Negative Breast Cancer \| Breast Cancer 3	6	Atorvastatin+xeloda (Cohort 1a)	mlzvbmesnx(uvyogewuro) = odeikvdjqe dmxrwaksvw (dqevcupnpx, eooldnuvnm - kxxmsmrudh) View more	-	02 Oct 2024
				Atorvastatin+xeloda (Cohort 1b)	mlzvbmesnx(uvyogewuro) = veplnzlkcu dmxrwaksvw (dqevcupnpx, pizxdxcxmj - gdywlrybmc) View more
ESC2024	Not Applicable	Cerebral Hemorrhage	-	Atorvastatin	livlpxjcnc(aqnttglrhz) = totprcxtsp iuvjjacxxx (ukfonyfeky ) View more	Negative	31 Aug 2024
				Vehicle	livlpxjcnc(aqnttglrhz) = rwkehpvttw iuvjjacxxx (ukfonyfeky ) View more
EUCTR2015-001808-57-ES \| NCT02679261 (Pubmed)	Phase 3	Bicuspid Aortic Valve Disease	220	Atorvastatin 20 mg/day	bjxdsoobwf(lnisebnbtw) = yghdvqihnb jqzotirsrn (dtaznkjfld, -51.65 to -1.75)	Negative	18 Jun 2024
				Placebo	bjxdsoobwf(lnisebnbtw) = sfugxibnkd jqzotirsrn (dtaznkjfld, -4 to 22.5)
NCT05331053 (CTgov)	Phase 4	Endometriosis	6	Atorvastatin	kmdbxqhwnk(owhenkxrzn) = lyehpadglr nugwoqysxi (wksoktluod, jxcadmhqzk - iqvfxsbbuv) View more	-	28 Feb 2024
NCT04952350 (Clinical Trial Registry, Pubmed \| Respir Res)	Phase 3	COVID-19	220	Atorvastatin 40 mg	mcbzgwiqxo(vcvxcvdyro) = zsaemmnhfn fvcmeprfcd (cllmotxtqj ) View more	Negative	22 Feb 2024
				Placebo	mcbzgwiqxo(vcvxcvdyro) = lzgxcpbhdp fvcmeprfcd (cllmotxtqj ) View more
NCT02943590 (CTgov)	Phase 2	Cardiotoxicity \| Heart Failure	300	Placebo (Placebo)	jcxlgtrtar(znntgzwjgr) = htqisqiazv rflyhshcna (jmoxqucrqg, tegwzmrviw - wzpcviqnut) View more	-	18 Dec 2023
				Atorvastatin (Atorvastatin)	jcxlgtrtar(znntgzwjgr) = ukjwdyjxfa rflyhshcna (jmoxqucrqg, popmedezdu - ucfigbkrsh) View more
NCT05730634 (Pubmed \| Diabetologia)	Not Applicable	Diabetes Mellitus, Type 2	24	Atorvastatin 40 mg	hzyaraojha(qrbjfgbykh) = zxgdyasikh jewoguzzyw (hpslhgrqfb ) View more	-	15 Aug 2023
NCT00701220 (CTgov)	Phase 4	Non-ischemic Cardiomyopathy \| Myocardial Ischemia	9	Atorvastatin Calcium	zobqffugdn(neimwzsdom) = vfjxkyncbu jzdvsnxkgr (dnfqodmgqe, qfdolbqkys - obszxklryz) View more	-	18 Jul 2023

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