Effects of Acetyl L-Carnitine Supplementation on Clinical, Metabolic and Inflammatory Symptoms in Obese, Diabetic, Postmenopausal Women With Osteoarthritis: Randomized Controlled Trial

OA is a degenerative bone disease more common in postmenopausal women. Diabetes and obesity are common risk factors for the development of OA. The common symptoms include pain and disability of the affected joint, leading to mobility issues. Acetyl L-carnitine due to its known anti-inflammatory, chondroprotective, and improved insulin-sensitizing effects may help in alleviating the symptoms and progression of OA in obese diabetic postmenopausal women.

Start Date01 Dec 2025

Sponsor / Collaborator

Khyber Medical University

CTRI/2025/05/087479

/ Not yet recruitingPhase 1/2IIT

Adjunctive Treatment with Acetyl-L-carnitine for Cognitive and Negative Symptoms in Schizophrenia: A RCT - prospective trail

Start Date07 Aug 2025

Sponsor / Collaborator-

NCT06126315

/ RecruitingPhase 2/3IIT

A Randomized, Phase II/III Trial on the Biological and Clinical Effects of Acetyl-L-carnitine in ALS

Phase II/III multicenter, randomized, double-blind, placebo-controlled trial on acetyl-L-carnitine (ALCAR) in subjects living with amyotrophic lateral sclerosis (ALS). Primary study aim: The clinical objective consists of assessing the efficacy of ALCAR (two different dosages will be tested: 1.5g/day and 3g/day) on the progression of functional disability (loss of self-sufficiency), as measured by the ALSFRS-R scale. Secondary study aims: 1. The effect of ALCAR treatment on different clinical aspects: functional decline as measured by ALSFRS-R total score; the decline of forced vital capacity (FVC); quality of life as measured by ALSAQ-40 scale; cognitive function as measured by Edinburgh Cognitive and Behavioural ALS Screen (ECAS) scale; survival (being alive and without tracheostomy). 2. To measure the effects of ALCAR treatment on disease biomarkers potentially involved in the drug's mechanisms of action. These include PGC-1 alpha, 3-nitrotyrosine (3-NT), acetyl cyclophilin A (acetyl-PPIA), neurofilament light chain (NFL), creatine kinase (CK), Musclin/osteocrin, MyomiRNA (MiR-206), Uric acid, Matrix metalloproteinase-9 (MMP-9), Monocyte Chemoattractant Protein-1 (MCP-1), 4-Hydroxynonenal (HNE). 3. The tolerability and safety of ALCAR treatment by identifying unexpected adverse events.
Study population: 246 subjects will be enrolled on one Australian and ten Italian ALS sites.
Inclusion criteria: subjects aged 18+ years with a diagnosis of ALS according to Gold Coast Criteria; disease duration <24 months; satisfactory bulbar and spinal function (self-sufficiency evaluated by a score 3+ on the ALSFRS-R for swallowing, cutting food and handling utensils, and walking); satisfactory respiratory function (FVC ≥80% of predicted); documented progression of symptoms as measured by the ALSFRS-R scale. Disease progression rate (DFS) must be>= 0.33. DFS =(48- ALSFRS-R at screening)/months from onset to screening, treatment with Riluzole in the last four weeks. Exclusion criteria: antecedent polio infection; other motor neuron disease; involvement of other systems possibly determining a functional impairment; other severe clinical conditions; unwillingness or inability to take riluzole; previous use of ALCAR for any reason; inability to understand and comply with the study requirements, and to give written informed consent personally or via their legally authorized representative.
All eligible participants will be randomized to receive ALCAR (1,5 or 3 g/day) or placebo in addition to riluzole 50 mg b.i.d. Permuted block (with a block size of 6), 1:1:1 centralized randomization scheme will be used. The overall treatment duration will be 48 weeks. After enrolment, each participant will be followed up until death. Eligible subjects will be seen after 4, 12, 24, 36 and 48 weeks. At each visit, a general assessment will be made, including vital signs, body mass index (BMI), neurological examination (including quantitative and qualitative evaluation of the motor system), comorbidity, concomitant treatments and adverse events. Blood samples will be collected at baseline -Day 1 (randomization)-, 4, 12, 24, 36 and 48 weeks to test biomarkers. Functional disability will be assessed at each visit using the ALS-FRS-R scale. The respiratory function will be assessed using a spirometer to measure FVC before starting treatment (baseline visit) and at 4, 12, 24, 36 and 48 weeks. Cognitive function will be evaluated at baseline, weeks 24 and 48, using ECAS scale. Health-related quality of life, measured by the ALSAQ-40, will be tested at baseline, 24 and 48 weeks. Compliance will be tested by the local investigators, counting unused packages at each follow-up visit. Pre-planned statistical analyses will be done on Intention-to-treat and Per-protocol (PP) populations. The statistical plan will include descriptive statistics and a comparison of the proportions of self-sufficient participants at week 48 using the chi-square or Fisher's exact test for the primary endpoint. Secondary endpoints measured by numerical scores obtained from clinical scales will be analyzed using repeated measures mixed models, while biomarkers using repeated measures ANOVA. Time-to-event endpoints, such as survival and the probability of remaining self-sufficient over 48 weeks, will be analyzed with Kaplan-Meier curves. The number of adverse events and serious adverse events after 48 weeks will be compared between treatment arms.

Start Date26 Mar 2025

Sponsor / Collaborator

Istituto di Ricerche Farmacologiche Mario Negri

[+2]

100 Clinical Results associated with Acetyl-L-carnitine

100 Translational Medicine associated with Acetyl-L-carnitine

100 Patents (Medical) associated with Acetyl-L-carnitine

3,395

Literatures (Medical) associated with Acetyl-L-carnitine

01 Nov 2026·INTERNATIONAL IMMUNOPHARMACOLOGY

Integrative transcriptomic analysis links epithelial PCK1 dysregulation to ulcerative colitis and acetyl-l-carnitine-mediated inflammatory modulation

Article

Author: Duan, He ; Rong, Wei ; Li, Yanrong ; Li, Yongzhuo ; Yu, Kangqian ; Hu, Yinan

BACKGROUND:

Ulcerative colitis (UC) is a chronic inflammatory disorder characterized by persistent mucosal injury and disturbed immune-metabolic homeostasis. Increasing evidence indicates that metabolic remodeling of intestinal epithelial cells contributes to UC-associated inflammation; however, the key metabolic regulators involved in this process remain poorly characterized.

METHODS:

Integrative analyses of bulk transcriptomic datasets from the Gene Expression Omnibus (GEO) were performed to identify UC-associated differentially expressed genes. Weighted gene co-expression network analysis (WGCNA), combined with intersection against an adipogenesis-annotated metabolic gene set, was used to identify candidate metabolism-associated DEGs. Machine learning algorithms were applied to develop an exploratory classification model and prioritize hub genes. Single-cell and spatial transcriptomics were employed to delineate cellular localization. Functional validation was performed in lipopolysaccharide (LPS)/tumor necrosis factor-α (TNF-α)-stimulated NCM460 cells and dextran sulfate sodium (DSS)-induced colitis mice, using siRNA-mediated knockdown of phosphoenolpyruvate carboxykinase 1 (PCK1) in vitro, pharmacological intervention with 3-mercaptopicolinic acid (3-MPA) in vivo, and acetyl-l-carnitine (ALC) treatment.

RESULTS:

Integrative transcriptomic analysis identified 11 metabolism-associated differentially expressed genes enriched in metabolism- and inflammation-related pathways, particularly AMP-activated protein kinase (AMPK) signaling. Machine-learning-based feature prioritization highlighted five candidate genes, with PCK1 showing the highest contribution to model prediction based on mean absolute SHapley Additive exPlanations (SHAP) values. PCK1 was downregulated in UC, with epithelial enrichment in single-cell analysis and spatially heterogeneous expression in inflamed mucosa. In functional assays, siRNA-mediated PCK1 knockdown enhanced inflammatory gene responses in vitro, while systemic 3-MPA treatment was associated with aggravated DSS-induced inflammatory phenotypes in vivo. ALC treatment partially restored PCK1 expression and alleviated inflammatory responses, with AMPK phosphorylation associated with its protective effects.

CONCLUSIONS:

PCK1 is an epithelial metabolism-associated candidate linked to inflammatory responses in UC. ALC treatment partially restored PCK1 expression and alleviated inflammatory responses, with AMPK phosphorylation associated with its anti-inflammatory effects.

01 Sep 2026·JOURNAL OF MOLECULAR MODELING

Theoretical evaluation of the antiradical activity of 1-Hydroxy-anhydrolycorin-7-one and anhydrolycorin-7-one from Lycoris aurea

Article

Author: Son, Nguyen Thi ; Ha, Nguyen Xuan

CONTEXT:

The antiradical activity of 1-hydroxy-anhydrolycorin-7-one (HAlc) and anhydrolycorin-7-one (Alc), two alkaloids isolated from Lycoris aurea, was theoretically investigated toward HOO• radical scavenging in aqueous and lipid-like environments. Thermodynamic analysis showed that HAlc is more favorable than Alc as a radical scavenger, mainly due to the additional hydroxyl group, which enhances both hydrogen atom donation and deprotonation ability. Among the investigated sites, the 2-OH group of HAlc displayed the lowest BDE and PA values and the most negative Gibbs free energy changes, indicating its key role in radical quenching. In pentyl ethanoate, HAlc scavenges HOO• predominantly through the fHAT mechanism at the 2-OH position, with an overall rate constant of 4.29 × 10⁶ M⁻¹ s⁻¹, approximately two orders of magnitude higher than that of Alc. In water, acid-base speciation strongly affects the scavenging mechanism. Although the neutral forms are dominant at physiological pH, the minor monoanionic species govern the overall kinetics through a highly efficient SET pathway. HAlc exhibited an overall aqueous rate constant of 3.04 × 10⁸ M⁻¹ s⁻¹, about 16 times higher than Alc and higher than common antioxidant references such as Trolox and ascorbic acid. These results identify HAlc as a promising natural antiradical agent, especially under physiological aqueous conditions.

METHODS:

All calculations were performed using Gaussian 09. The most stable conformers were optimized by density functional theory at the M06-2X/6-311++G(d,p) level. Solvent effects were described using the SMD model with water and pentyl ethanoate. The fHAT, SETPT, and SPLET mechanisms were evaluated using BDE, IP, PA, and reaction Gibbs free energies. Kinetic calculations were carried out following the QM-ORSA protocol. Transition states for fHAT reactions were confirmed by single imaginary frequencies associated with hydrogen transfer, tunneling corrections were included, and SET activation barriers were estimated using Marcus theory. Apparent and overall rate constants were calculated by considering acid-base molar fractions at pH 7.4.

01 Sep 2026·NEURON

Glucose hypometabolism and hyperphosphorylated Tau synergistically drive neuronal necroptosis

Article

Author: Yuan, Junying ; Chen, Xiaoshi ; Shan, Bing ; Li, Xiang ; Brendel, Matthias ; Liu, Jianping ; Neubauer, Antonia ; Liu, Jixuan ; Zou, Chengyu ; Li, Sixuan ; Zhang, Mengmeng ; Yang, Chongzhe ; Mao, Wei ; Herms, Jochen ; Liu, Cong ; Xu, Ruisheng

The combination of brain glucose hypometabolism and hyperphosphorylated Tau (p-Tau) pathology is the strongest known clinical predictor of imminent cognitive decline, yet how these factors cooperate to drive dementia remains unknown. Here, we show that glucose hypometabolism synergizes with p-Tau to trigger neuronal loss through necroptosis. Under low-glucose conditions, accumulated p-Tau forms a molecular scaffold that directly recruits RIPK1, while concomitant loss of the necroptosis checkpoint A20 removes a critical brake on this death pathway. This dual mechanism thereby precipitates neuronal necroptosis. Restoring A20 expression with acetyl-L-carnitine or preventing the p-Tau-RIPK1 interaction using a RIPK1-derived competitive peptide alleviates neuronal necroptosis and brain atrophy in a Tau transgenic mouse model. Collectively, our findings uncover a previously unrecognized metabolism-driven necroptotic signaling cascade initiated by a p-Tau-RIPK1 hub, providing mechanistic insight into how glucose hypometabolism synergizes with p-Tau to drive neurodegeneration.

News (Medical) associated with Acetyl-L-carnitine

27 Jan 2025

·www.prnewswire.com

Blue Toad Botanicals Launches You've Got Some NERVE™ Stack Featuring Vanizem™ Aframomum melegueta Extract

Synergistic Formulation Designed to Support Healthy Nerve Function MORRISTOWN, N.J., Jan. 27, 2025 /PRNewswire/ -- PLT Health Solutions, Inc. announced that Blue Toad Botanicals™ (Boise, ID USA), a premium lifestyle brand that delivers targeted therapeutic functional mushrooms and botanical stacks has launched a new consumer health product called You've Got Some NERVE™ Functional Mushroom Capsules. The product features PLT Health Solutions' Vanizem™ Aframomum melegueta, which has been clinically demonstrated to improve mood and sleep. The complex formulation for You've Got Some NERVE™ consists of functional mushrooms and a broad range of cutting-edge botanicals and vitamins. This one-of-a-kind stack includes a potent blend of Neuro AEA™ (Anandamide & Myristicin), Feverfew, Passion Flower, Skullcap, Neuro AGARIC™ (Muscimol), Methylated B-Complex, Benfotiamine, Proprietary Terpene Stack and Acetyl-L-Carnitine. Continue Reading You've Got Some NERVE™ consists of functional mushrooms and a broad range of cutting-edge botanicals and vitamins. This one-of-a-kind stack includes a potent blend of NeuroAEA™ (Anandamide & Myristicin), Feverfew, Passion Flower, Skullcap, NeuroAGARIC™ (Muscimol), Methylated B-Complex, Benfotiamine, Proprietary Terpene Stack and Acetyl-L-Carnitine. Vanizem is a proprietary selection and extraction of the West African flowering plant Aframomum melegueta (Grains of Paradise) with standardized bioactives, including 10% vanilloids where 1.5% of them are 6-Paradol that target the endocannabinoid system. Launched in January 2025, You've Got Some NERVE™ is available direct-to-consumer via the Internet and at . According to Co-founder & CEO/Chief Innovation Officer Paul Frantellizzi of Blue Toad, the development and launch of this new product is in line with the company's mission to offer premium quality ingredients with quality science that consumers will actually feel when they consume them. "Living with nerve issues can be challenging and can take a significant toll on people's quality of life. It can affect mood, sleep and impact overall quality of life. Our goal is to empower people to take a more active role in their health and lifestyle and discover effective strategies for supporting neurologic health. Informing the development of this product was my own history of struggling with these issues, he said. The addition of a branded, clinically studied ingredient like Vanizem to this formulation helps us build trust with our customers and offers new, disruptive benefits to our product. We were extremely excited about the standardized content of 10% vanilloids," he added. Vanizem: A unique botanical solution Vanizem is a proprietary selection and extraction of the West African flowering plant Aframomum melegueta (Grains of Paradise) with standardized bioactives, including 10% vanilloids where 1.5% of them are 6-Paradol that target the endocannabinoid system. In a recently completed clinical study, Vanizem was shown to provide improvements in self-reported tension scores (POMS) and significant improvements in sleep quality score (LSEQ) along with improvements in mood, vigor, ease of falling asleep and easier morning awakening.* Studies showed that a low dose showed significant results in improving mental wellbeing, reducing stress and anxiety levels, supporting sleep and contributing to overall relaxation.within just three days.* The ingredient was developed by PLT innovation partner Nektium Pharma (Las Palmas, Spain). PLT Health Solutions is the exclusive sales and marketing partner for Vanizem in North America. According to Steve Fink, Vice President of Marketing for PLT Health Solutions, Blue Toad is an exciting and innovative company in the health and wellness space. "The team at Blue Toad 'get' what self-care through the use of botanicals is all about. They were one of the first companies that recognized the potential for Vanizem. We are excited at the launch of this new product and look forward to more people being introduced to the benefits of Vanizem," he said. For more information on Blue Toad Botanicals, visit bluetoadbotanicals.com For more information on Vanizem, visit plthealth.com/vanizem *These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease. Blue Toad Botanicals™ products are not intended to diagnose, treat, cure, or prevent any medical disorder or disease. About Blue Toad Founded in early 2021 by Pamela Peters & Paul Frantellizzi, Blue Toad™ is a Boise-based, award-winning, and extremely disruptive team of industry professionals developing premium functional-mushroom and targeted therapeutic microdose stacks that solve consumer problems. We understand that gut-health is key to homeostasis & building upon that premise, we use patented, clinically validated ingredients & botanical stacks giving consumers need-state support for Mood, Pain, Sleep, Anxiety, Hormones, Immunity, etc. Blue Toad™ is currently well positioned to be the next big brand in the functional mushroom & wellness industry. About PLT Health Solutions Headquartered in Morristown, NJ, USA, PLT Health Solutions is a trusted discoverer, developer, and marketer of high-quality, scientifically supported ingredients that enhance health and functionality. As a leading ingredients innovator, PLT's global network of strategic partnerships provides unique access to impactful solutions. PLT Health Solutions is a purpose-driven company passionate about helping people live healthier, happier lives. By delivering an unsurpassed mix of expertise, resources, and service, PLT is committed to helping both its strategic partners and valued customers grow. SOURCE PLT Health Solutions WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

08 Jan 2025

·www.prnewswire.com

Study Advances Possible Blood Test for Early-Stage Alzheimer's Disease

Findings may explain why women are at higher risk NEW YORK, Jan. 8, 2025 /PRNewswire/ -- Declining blood levels of two molecules that occur naturally in the body track closely with worsening Alzheimer's disease, particularly in women. Levels were found to drop gradually, from women with no signs of memory, disorientation, and slowed thinking to those with early signs of mild cognitive impairment. Decreases were more prominent in women with moderate or severe stages of the disease. Declines in men were evident in only one molecule, revealing a disease-specific difference between the sexes. Six million Americans, most over the age of 65 and predominantly women, are currently estimated to have some form of Alzheimer's disease. Led by neuroscientists at NYU Langone Health, in collaboration with other researchers in the U.S. and Brazil, the new study showed that blood levels of the protein acetyl-L-carnitine were lower in both women and men with mild cognitive impairment and Alzheimer's disease. Blood levels of free carnitine, the main byproduct of acetyl-L-carnitine in reactions essential to brain function, steadily declined in women in amounts related to the severity of their cognitive decline. In men, significant declines were seen only in acetyl-L-carnitine, not free carnitine. Published in the journal Molecular Psychiatry online Jan. 7, the study results suggest that declines in these two brain chemicals could indicate the presence and degree of Alzheimer's disease, and that this difference might offer an explanation as to why women are at higher risk of the disease than men. Additional computer testing showed that blood levels of acetyl-L-carnitine and free carnitine aligned in direct proportion in study participants to increased amyloid beta and tangled tau protein levels, long considered markers of progressive severity in Alzheimer's disease. Indeed, the research team's accuracy in diagnosing the severity of Alzheimer's disease rose from more than 80% – when using either amyloid beta and tangled tau protein levels collected from cerebrospinal fluid or the two blood molecules – to 93% when using both. "Our findings offer the strongest evidence to date that decreased blood levels of acetyl-L-carnitine and free carnitine could act as blood biomarkers for identifying those who have Alzheimer's disease, and potentially those who are at greater risk of developing early dementia," said study lead investigator Betty Bigio, PhD. "The results also might explain the differences by sex in Alzheimer's disease, with more women than men having dementia," said Bigio, a research assistant professor in the Department of Psychiatry at NYU Grossman School of Medicine. Bigio is also affiliated with the Nathan Kline Institute for Psychiatric Research. "Because declines in acetyl-L-carnitine and free carnitine tracked closely with the severity of Alzheimer's disease, the molecular pathways involved in their production offer other possible therapeutic targets for getting at the root cause of the disease and potentially intervening before permanent brain damage occurs," said senior study investigator Carla Nasca, PhD. Nasca is an assistant professor in the Departments of Psychiatry and Neuroscience at NYU Grossman School of Medicine. Nasca is also affiliated with the Nathan Kline Institute for Psychiatric Research. The study involved data on two separate groups of men and women in Brazil and California, in which the researchers measured blood levels of the two molecules. A total of 93 study volunteers diagnosed with varying degrees of cognitive impairment were involved, along with 32 cognitively healthy men and women of similar age, weight, and education. Results in the Californian group were used to confirm what was found in the Brazilian group. Moving forward, Nasca says more research is needed into the root sources of acetyl-L-carnitine and the molecular pathways that control its production and into tracking how the molecule affects brain chemistry as it is contained in brain vesicle stores released into the blood. The team's goal is to define other biomarkers in the brain that track closely with Alzheimer's disease progression. If further studies confirm their latest findings, Nasca says the team's research could be used to develop a blood test for dementia and for tracking the progression of Alzheimer's disease in an easier and noninvasive way. Currently, searching for biomarkers of disease progression can involve serial spinal taps that pose risks of pain and infection. A blood test might also be useful to support or add a more objective, quantitative measure of disease severity than existing questionnaires that test memory or thinking skills. A blood test, Nasca says, could also help predict the effectiveness, or lack thereof, of potential new drug treatments designed to delay or prevent the onset of Alzheimer's disease. Both acetyl-L-carnitine and free carnitine are essential for healthy brain function and regulating cell energy metabolism. Past research by Nasca's team showed that acetyl-L-carnitine also shuttles molecules from a cell's powerhouse mitochondria to a cell's controlling nucleus, allowing genes to open and become activated. This shuttling action is key in regulating genes that produce the neurotransmitter glutamate, another chemical involved in most brain activities, including nerve cell repair (plasticity). This matters in the hippocampus region of the brain, which helps regulate memory and where initial damage from Alzheimer's diseases is known to appear. Nasca says that excessive levels of glutamate have also been tied to mood disorders and severe cases of depression in humans, disorders closely tied to Alzheimer's disease. Her team has also linked deficiencies in acetyl-L-carnitine, but not free carnitine, to depression and childhood trauma. Future investigations are planned about how to prevent the progression of depression to Alzheimer's disease. Funding support for the study was provided by National Institutes of Health grants R24AG06517, P50AG16573, and P30AG066519. Additional funding support came from the Robertson Therapeutic Development Fund, D'Or Institute for Research and Education, Rede D'Or Sao Luiz Hospital Network, International Society for Neurochemistry, Fundacao Carlos Chagas Filho de Ampara a Pesquisa do Estado do Rio Janeiro, Serrapilheira Institute, and Alzheimer's Association grant AARG-D-61541. Besides Bigio and Nasca, other NYU Langone researchers involved in the study are co-investigators Aryeh Korman and Drew Jones. Other study co-investigators are Ricardo Lima-Filho, Felipe Sudo, Claudia Drummond, Naima Assuncao, Bart Vanderborght, Sergio Ferreira, Paulo Mattos, Fernanda Tovar-Moll, Fernanda De Felice, and Mychael Lourenco, at the Federal University of Rio de Janeiro and the D'Or Institute for Research and Education, also in Brazil; Olivia Barnhill, at Rockefeller University in New York City; James Beasley and Sarah Young, at Duke University in Durham, N.C.; and David Sultzer and Elizabeth Head, at the University of California Irvine. About NYU Langone Health NYU Langone Health is a fully integrated health system that consistently achieves the best patient outcomes through a rigorous focus on quality that has resulted in some of the lowest mortality rates in the nation. Vizient, Inc., has ranked NYU Langone the No. 1 comprehensive academic medical center in the country for three years in a row, and U.S. News & World Report recently placed nine of its clinical specialties among the top five in the nation. NYU Langone offers a comprehensive range of medical services with one high standard of care across six inpatient locations, its Perlmutter Cancer Center, and more than 300 outpatient locations in the New York area and Florida. With $14.2 billion in revenue this year, the system also includes two tuition-free medical schools, in Manhattan and on Long Island, and a vast research enterprise with over $1 billion in active awards from the National Institutes of Health. Media Inquiries: David March 212-404-3528 [email protected] STUDY LINK SOURCE NYU Langone Health System WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical Result

06 Feb 2024

·www.prnewswire.com

Recognize National Senior Independence Month by Supporting Your Vitality With Gundry MD Energy Renew

A Dietary Supplement That Helps Recharge Your Energy and Fight Visible Signs of Aging LOS ANGELES, Feb. 6, 2024 /PRNewswire/ -- February is National Senior Independence Month. It is dedicated to empowering our senior community with the tools and knowledge to achieve well-being and vitality. Dr. Steven Gundry, a cardiothoracic surgeon and renowned expert in health and nutrition, provides invaluable tips to help maintain independence and vitality at any age. Continue Reading Gundry MD Energy Renew is a dietary supplement crafted with the delightful flavors of passionfruit and hibiscus. This specially crafted supplement is designed to help bolster your body's cell vitality, enabling the generation of energy. Formulated with the finest ingredients, including an exclusive polyphenol blend, Gundry MD Energy Renew cannot only support healthy energy levels but also help promote sustained wakefulness and mental clarity, aiding in your daily recovery. Navigating the natural changes that come with aging, like pains and decreased energy, can be challenging. But, Dr. Gundry teaches that aging does not have to equate to this. His motto is to help people 'die young at a ripe old age.' Dr. Gundry emphasizes three key tips to support longevity and vitality: Exercise Snacking: Incorporating short bursts of physical activity throughout the day, or as he likes to call it, "exercise snacking" Exercise snacking is a powerful way to boost energy levels and enhance overall well-being. Simple, quick exercises can make a significant difference in maintaining mobility and vitality, such as doing squats while brushing your teeth, dancing in your living room to an entire song, or leg or calf raises while you're watching TV Gut-Buddy Friendly Diet: Dr. Gundry advocates for a diet that feeds your good gut bacteria and starves the bad bacteria. Eat foods with soluble fiber, like asparagus and pressure-cooked beans. Incorporate fermented foods, like sauerkraut and sugar-free coconut yogurt, daily. And avoid sugary, highly processed foods. Take Supplements: To further support your energy levels and vitality, Dr. Gundry recommends using Gundry MD Energy Renew. This unique supplement features a robust blend of superfruits and hibiscus, combined with D-Ribose and Acetyl L-Carnitine. These ingredients work synergistically to support your energy stores and combat the unpleasant discomfort that comes with aging.†* Energy Renew also boasts a distinctive blend of superfruit extracts, delivering a mega-boost of polyphenols. These compounds act as powerful antioxidants and help "rewind the clock" and offer support to tired, aging cells. By incorporating Gundry MD Energy Renew into your daily routine, you can take proactive steps towards maintaining independence and embracing the joys of aging with vitality.†* What is Gundry MD Energy Renew? Gundry MD Energy Renew is a passion fruit-flavored dietary supplement designed to unleash the benefits of its unique blend of ingredients, promoting youthful energy and vitality. This powerful formula includes superfruits and hibiscus, coupled with D-Ribose and Acetyl L-Carnitine, working harmoniously to help boost cellular energy without the risk of crashing. Within Gundry MD Energy Renew, superfruits flood your body with antioxidants, supporting the immune system and facilitating easier weight management. Meanwhile, the combination of D-Ribose and Acetyl L-Carnitine enhances alertness throughout the day, promoting a youthful feeling and contributing to healthy-looking skin. This well-balanced blend of potent energy boosters and superfruits serves as an ideal pick-me-up for those grappling with exhaustion, weakness, or premature visible aging. Gundry MD Energy Renew also features healthy compounds capable of virtually support aging cells. This unique aspect of the supplement can help foster independence and mobility as you age, making it a comprehensive solution for your overall well-being.†* Where to Purchase Gundry MD Energy Renew Gundry MD Energy Renew can be purchased on the Gundry MD website for the cost of $74.95 for a 30-day supply with a 90-day purchase price guarantee. Suggested Use of Gundry MD Energy Renew Gundry MD Energy Renew can be effortlessly prepared by mixing one scoop of the passionfruit-hibiscus flavored powder with 8 oz. of water. You can incorporate this supplement into your routine at any time of day. Simply mix, sip, and experience the revitalizing benefits of Gundry MD Energy Renew. About Gundry MD Founded in 2015, Gundry MD is dedicated to providing cutting-edge solutions to its users by using science-backed ingredients that can offer a boost in metabolism, all-day energy, smooth, easy digestion, and a youthful-feeling mind and body. These amazing results all begin with feeding your body powerful health-boosting nutrients like polyphenols. Based on his many years of nutrition research, Dr. Gundry helps create every Gundry MD product. Best-selling Gundry MD products include Total Restore, Energy Renew, and Polyphenol-Rich Olive Oil. All Gundry MD products come with a 90-day purchase price guarantee if you are not satisfied. For more information, visit or @gundrymd on Instagram and Facebook.† About Dr. Gundry Founder of Gundry MD, Dr. Steven Gundry was one of the world's top cardiothoracic surgeons and is currently the medical director at The International Heart and Lung Institute and The Centers for Restorative Medicine in Palm Springs, Beverly Hills, and Santa Barbara, California. He has spent the past 25 years helping people restore their health by optimizing nutrition and lifestyle choices. Steven Gundry, MD is also the host of the top-ranked health podcast, The Dr. Gundry Podcast, and author of four New York Times best-selling books including The Plant Paradox™ which details his famous lectin-free Plant Paradox Diet. His new book Gut Check provides the keys to unlocking our gut health, allowing our bodies, and their microbiome, to function at their highest potential. For more information, visit drgundry.com and the Dr. Gundry YouTube channel, and follow @drstevengundry on Instagram and TikTok. *All individuals are unique. Your results can and will vary. Media Contact: Ashley Beenen [email protected] SOURCE Gundry MD

100 Deals associated with Acetyl-L-carnitine

External Link

KEGG	Wiki	ATC	Drug Bank
-	Acetyl-L-carnitine	N06BX12	DB08842

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Peripheral Nervous System Diseases	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	05 Jan 1997
Dementia	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	31 Dec 1996
Diabetic Neuropathies	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	23 Feb 1995
Alzheimer Disease	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	28 Jan 1995

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	Phase 3	Italy	Leadiant Biosciences, Inc.	01 Apr 2008
Hypertension	Phase 3	Italy	Leadiant Biosciences, Inc.	01 Apr 2008
Breast Cancer	Phase 2	United States	Alfasigma SpA	01 Mar 2007
Reflex Sympathetic Dystrophy	Phase 2	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	25 May 2006
Acute Lymphoblastic Leukemia	Phase 2	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	21 Mar 2006
Neurotoxicity Syndromes	Phase 2	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	21 Mar 2006
Sensory neuropathy	Phase 2	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	21 Mar 2006
HIV-Associated Lipodystrophy Syndrome	Phase 2	Italy	Sigma-Tau Industrie Farmaceutiche Riunite SpA	17 Mar 2006
Diabetes Complications	Phase 2	Japan	Tanabe Pharma Corp.	-
Fatigue	Phase 2	United States	Sigma-Tau Industrie Farmaceutiche Riunite SpA	-

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


EHA2026	Not Applicable	Acute Myeloid Leukemia	188	IC "3+7" regimen	mkvutkkzpt(sehcplqrru) = bveuvqkmjj gyotodeoen (vypfmcgrdq )	Positive	12 May 2026
				Fludarabine-based IC	mkvutkkzpt(sehcplqrru) = kmujwmtlxt gyotodeoen (vypfmcgrdq )
NCT01695317 (EUDRACT (2012-001624-36) \| ALCAR, CTgov)	Phase 4	Migraine Disorders \| Migraine Without Aura	72	Acetyl-L-carnitine (Acetyl-L-carnitine)	ssmeynzpyn(slpzrjstvf) = dbpjbgwojw ufvgansmdm (vzbcldvuzk, 2.8) View more	-	13 Apr 2022
				Acetyl-L-carnitine (Sugar Pills)	ssmeynzpyn(slpzrjstvf) = bvbesuoetz ufvgansmdm (vzbcldvuzk, 3.3) View more
NCT01054768 (CTgov)	Phase 2	Inflammation \| Anemia, Sickle Cell	37	alpha-lipoic acid+acetyl-L-carnitine (Alpha-lipoic Acid and Acetyl-L-carnitine)	bangjyzgwc(oslknyawwr) = tbcxrnxedc zseaxnoafk (zmwawrxrsq, 20.9) View more	-	03 Aug 2021
				Control (Placebo)	bangjyzgwc(oslknyawwr) = yqwqubgojh zseaxnoafk (zmwawrxrsq, 10.3) View more
NCT03297944 (CTgov)	Phase 4	Psychomotor Disorders	15	Placebo (PLC/PLC)+ZOL+PLC+Alprazolam+Zolpidem+ALC	uxxphxrpwu(nqrkhvgoyb) = bbxcfiaukt akpgklaiad (sqzqjuszfd, ipnaoaeiga - oqhhvcuzjg) View more	-	29 Jan 2020
NCT00775645 (SWOG S0715 \| S0715, ASCO2017)	Phase 3	Peripheral Nervous System Diseases	437	Acetyl-L-Carnitine	vasaxzyoid(rfhzhggfxj): P-Value = 0.01 View more	Negative	30 May 2017
				Placebo
NCT05601479 (Pubmed \| Exp Ther Med)	Phase 2	Chemotherapy-induced damage	239	Acetyl-L-carnitine	nnexcccwvs(woiidmvqgm) = wputyshmay jtsefxxvsd (hrnzupyovx )	Positive	01 Dec 2016
				Placebo	nnexcccwvs(woiidmvqgm) = gwwoaiolww jtsefxxvsd (hrnzupyovx )
NCT02485158 (TDS, CTgov)	Not Applicable	-	28	placebo+d-amphetamine+amphetamine+THC (AMP Arm)	vmijfvsydn(epvixnbbsw) = etiscgmnie hkepambcda (gkfqfutyfp, 7.22) View more	-	29 Nov 2016
				placebo+d-amphetamine+THC (ALC Arm)	vmijfvsydn(epvixnbbsw) = gglekmpnwo hkepambcda (gkfqfutyfp, 18.78) View more
NCT01695317 (EUDRACT (2012-001624-36), Pubmed \| Cephalalgia)	Phase 4	Migraine Disorders	72	Acetyl-l-carnitine	xlewkypdha(sezcqeupjo) = kdszthljsc qlxhwegifq (znuysaicde )	Negative	01 Oct 2015
				Placebo	xlewkypdha(sezcqeupjo) = ydtswsziyj qlxhwegifq (znuysaicde )
Pubmed \| Amyotroph Lateral Scler Frontotemporal Degener	Not Applicable	Amyotrophic Lateral Sclerosis	-	Acetyl-L-carnitine 3g/day	nudkunqdrt(ynosecqvqx) = xolytagemk wwerohlgsk (kvnfkbigbk, 10.4) View more	Positive	01 Sep 2013
				Placebo	nudkunqdrt(ynosecqvqx) = wshkppunpl wwerohlgsk (kvnfkbigbk, 9.9) View more
NCT00719706 (CTgov)	Phase 2	Bipolar Disorder	40	alpha-lipoic acid+acetyl-l-carnitine (ALCAR/ALA)	wybvareztf(ugqdfqvtyh) = sqmdihpird byynfpgcbi (ovclcbdell, 3.5) View more	-	18 Jul 2012
				placebo (Placebo)	wybvareztf(ugqdfqvtyh) = uepmnspmdb byynfpgcbi (ovclcbdell, 3.2) View more

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