This is a 20-week study for children between 3 and 6 years old with confirmed childhood apraxia of speech (CAS). The study includes a 12-week open-label pilot feasibility study of an investigational drug (Omega-DEK) plus L-carnitine (Carnitor®), which is followed by an 8-week randomized, placebo-controlled discontinuation period among the same study participants.

Start Date01 May 2026

Sponsor / Collaborator

Emory University

CTIS2024-519366-52-00

/ RecruitingPhase 2

Pilot Study to Evaluate Safety and Efficacy of PolyCore, a Ternary Combination of Xylitol, L-Carnitine and Polydextrin, to Treat End-Stage Kidney Disease Patients Starting Peritoneal Dialysis (EXCITE)

Start Date17 Feb 2026

Sponsor / Collaborator-

NCT07402759

/ Active, not recruitingPhase 3IIT

Impact of tdrd9 Gene Mutations in the Therapeutic Response to L-carnitine in Oligoasthenozoospermic Men

Infertility remains a significant global burden. Estimates suggest that 10-15% of couples worldwide experience infertility, with male infertility being the underlying cause in 20-50% of cases. For the majority of cases however the etiology remains unknown, and is termed idiopathic infertility. Azoospermia, absence of spermatozoa in the semen, is one of the most common reasons for infertility in men, with a prevalence of 1% in the general population, and over 15% in infertile men.
Oligozoospermia is a major cause of male infertility, yet its genetic basis remains partially understood. Oligozoospermia refers to sperm concentrations below established reference limits (e.g. 16 million/ml, 95% confidence interval 15-18 million/ml; WHO 2021).
Numerous studies have demonstrated a strong genetic basis for oligozoospermia, with genetic abnormalities, such as abnormalities in chromosome number or structure, azoospermia factor region (AZF) deletion on the Y chromosome and cystic fbrosis transmembrane conduction regulator (CFTR) gene mutations, reported in men with otherwise unexplained oligozoospermia and azoospermia. Moreover, previous studies have identifed more than 400 genes that are specifcally or potentially associated with fertility regulation while potentially contributing to the widespread genetic heterogeneity associated with dyszoospermia. For example, mutations in RPL10L and MAGEB have been reported to cause oligozoospermia. However, mutations in only a few genes have been shown to cause male infertility, and the candidate pathogenic genes for oligozoospermia still need to be studied further.
Recent studies have implicated the Tudor Domain Containing 9 (TDRD9) gene in the regulation of spermatogenesis through its role in piRNA pathway and transposon silencing. A 2024 study identified compound heterozygous mutations-c.1115+3A>G (splicing variant) and c.958delC (frameshift variant)-in a Chinese family with idiopathic oligozoospermia, resulting in aberrant splicing and truncated TDRD9 protein products.
Tudor domain-containing protein 9 (TDRD9) is an RNA helicase that is highly expressed in germlines. TDRD9 expression has been detected in mitotic spermatogonia, meiotic spermatocytes and haploid spermatids in the testis. In male infertility cases, TDRD9 has been reported to be involved in the silencing of long intersperm-1 retrotransposons, suggesting an association between TDRD9 mutations and non-obstructive azoospermia.
TDRD9 is implicated in spermatogenesis and piRNA pathway integrity. Variants may affect sperm quality and response to treatments. L-carnitine is widely used as an antioxidant and metabolic supplement shown to improve sperm parameters in some infertile men. This study will test whether TDRD9 mutation status predicts therapeutic benefit from L-carnitine.

Start Date01 Jan 2026

Sponsor / Collaborator

South Valley University

100 Clinical Results associated with Levocarnitine

100 Translational Medicine associated with Levocarnitine

100 Patents (Medical) associated with Levocarnitine

12,907

Literatures (Medical) associated with Levocarnitine

31 Dec 2026·REDOX REPORT

Protective role of fatty acid oxidation against epithelial barrier dysfunction in allergic asthma

Article

Author: Chung, Kian Fan ; Yin, Huiming ; Gao, Shaoyong ; Gao, Jing ; Gao, Wei ; Wang, Muyun ; He, Yanan ; Li, Qiang ; Wu, Di ; Liao, Ximing ; Hu, Haiyang ; Wang, Kun

BACKGROUND:

Fatty acid oxidation (FAO) is implicated in lung diseases, but its role in bronchial asthma is not fully understood. We investigated its effect on airway epithelial barrier integrity.

METHODS:

Using a house dust mite (HDM)-induced murine asthma model and HDM, IL-4, IL-13, or TNF-α stimulated human primary bronchial epithelial cells (BECs) and bronchial epithelial (Beas-2b) cells, we modulated FAO with L-carnitine (agonist) and Etomoxir (inhibitor). BECs and Beas-2b cells were infected with lentivirus-mediated CPT1A shRNA prior to stimulation. Barrier function, mitochondrial oxidative stress, inflammation, and metabolism were assessed.

RESULTS:

FAO level in lungs negatively correlated with increased inflammation and tissue injury in HDM-induced asthmatic mice (all p < 0.05), while positively regulating tight junction protein expression. In BECs and Beas-2b cells, Etomoxir treatment and CPT1A knockdown exacerbated the impairment of FAO caused by various stimulants (all p < 0.05). Furthermore, FAO negatively regulated HDM/cytokine-induced epithelial barrier damage, hyperactive inflammatory response, and mitochondrial dysfunction in Beas-2b cells (all p < 0.05). In contrast, treatment with L-carnitine significantly alleviated these pathophysiological features in both in vivo and in vitro models.

CONCLUSION:

FAO plays a protective role in the occurrence and development of asthma by maintaining airway epithelial cell homeostasis and barrier function.

31 Dec 2026·Journal of the International Society of Sports Nutrition

A comprehensive review of the physiology and evidence base to guide the use of ergogenic and medical supplements for enhanced cycling performance

Review

Author: Edwards, Sophie ; Prieto-Bellver, Gorka ; Cornelisse, Erik ; Rowland, Angela ; Rowland, Andrew ; Hopkins, Ashley M ; Karapetis, Christos S ; Menz, Bradley ; Wallen, Matthew P

BACKGROUND:

A growing body of evidence supports the use of supplements to enhance cycling performance through both direct and indirect mechanisms.

METHODS:

This review was informed by a structured literature search conducted in PubMed, Scopus and Web of Science for peer-reviewed studies published up to May 2025. Studies were included if they involved human participants, were published in English and evaluated outcomes related to endurance performance, recovery or physiological function.

RESULTS:

Direct enhancement with ergogenic supplements is primarily achieved via modulation of skeletal muscle energy metabolism. During exercise, adenosine triphosphate (ATP) resynthesis is driven by the phosphagen system, glycolysis, oxidative phosphorylation and beta-oxidation, with each system contributing according to the intensity and duration of the effort. Supplements such as beta-alanine, caffeine, carbohydrates, carnitine, creatine monohydrate, dietary nitrates, electrolytes, exogenous ketones, N-acetylcysteine and sodium bicarbonate support these energy systems by improving substrate utilization, buffering capacity, energy availability or resistance to fatigue. In addition to ergogenic supplements that directly enhance performance, medical supplements play an important indirect role by supporting bone health, connective tissue integrity, inflammation management, micronutrient status, muscle repair and gut function. Evidence-based options for cyclists include calcium, cherry juice, collagen, curcumin, iron, multivitamins, omega-3 fatty acids, pickle juice, probiotics, protein, vitamin C, vitamin D and zinc. Each contribute to either improved recovery, immune support or long-term physiological adaptation. Evidence quality varied substantially across supplements, with strongest support for Australian Institute of Sport (AIS) Group A compounds. The integration of physiological testing including assessments of maximal oxygen consumption (VO₂max), lactate threshold, metabolic substrate utilization and blood biomarkers may inform the development of individualized supplementation strategies tailored to training demands and competitive goals.

CONCLUSIONS:

This evidence-informed approach underscores the synergistic relationship between nutrition, training and performance optimization in cycling. Future research should explore personalized nutrition frameworks, interactions between multi-supplement protocols and the molecular mechanisms underpinning adaptation to endurance training and nutritional interventions.

01 Apr 2026·JOURNAL OF APPLIED TOXICOLOGY

Monosodium Glutamate Exposure and Liver Damage: Modulatory Effects of L‐Carnitine on Inflammation and Autophagy

Article

Author: Pektas, Ferhat ; Kalkan, Kubra Tuğce

ABSTRACT:

Monosodium glutamate (MSG), a widely used flavor enhancer, has been associated with hepatotoxicity through mechanisms involving oxidative stress, inflammatory activation, and disruption of autophagy. L‐Carnitine, recognized for its antioxidant and anti‐inflammatory effects, has been proposed as a potential therapeutic agent against liver injury. This study aimed to evaluate the hepatotoxic effects of monosodium glutamate (MSG) and the therapeutic potential of L‐carnitine in mitigating MSG‐induced liver injury, with emphasis on autophagy‐related pathways. Forty male offspring obtained from 12 pregnant Wistar albino rats were divided into five groups ( n = 8 per group): control, sham, MSG, L‐carnitine, and MSG + L‐carnitine. Neonatal rats received MSG (4 g/kg, s.c.) on postnatal days 2, 4, 6, 8, and 10, whereas L‐carnitine (200 mg/kg, i.p.) was administered between postnatal days 60–81. Biochemical, histopathological, and immunohistochemical analyses were performed. MSG exposure significantly increased serum ALT levels ( p < 0.05) and caused marked histological alterations, including cytoplasmic vacuolization ( p < 0.001), eosinophilia ( p < 0.001), sinusoidal dilatation ( p < 0.001), and fibrosis ( p < 0.001). [Correction added on 13 January 2026, after first online publication: The phrase “AST (p<0.001) and ALT (p<0.001) levels” has been revised to “ALT levels (p<0.05)” in the previous sentence.] Immunohistochemically, MSG reduced mTOR immunoreactivity by 4% ( p < 0.05) while increasing ULK1 by 6% ( p < 0.01) and ATG13 by 3.5% ( p < 0.05). L‐Carnitine treatment significantly decreased histological damage scores (vacuolization −28%, fibrosis −25%, all p < 0.05), restored mTOR levels ( p > 0.05 vs. control), and attenuated ULK1 and ATG13 overexpression ( p < 0.01). These findings demonstrate that L‐carnitine exerts a therapeutic effect against MSG‐induced hepatocellular injury by modulating oxidative stress, inflammatory cytokines, and autophagy imbalance via the mTOR–ULK1–ATG13 pathway.

News (Medical) associated with Levocarnitine

12 Mar 2026

·endpoints.news

Lilly warns of impurity risk in certain compounded forms of Mounjaro and Zepbound

Compounded forms of the molecule behind Eli Lilly’s metabolic blockbusters Mounjaro and Zepbound that have vitamin B12 added to them may be unsafe, Lilly said Thursday. Lilly and its fellow GLP-1-based drugmaker Novo Nordisk have both taken a stance against compounding pharmacies, which make copycats of their drugs that sometimes include other molecules such as vitamin B12 to differentiate them from the branded versions. Lilly has sued compounders in the past, as has Novo . Lilly released a warning letter saying that tests had revealed “significant levels of an impurity that results from a chemical reaction between tirzepatide and B12.” It suggested that this impurity could pose risks, including toxicity and immune reactions, and added that patients taking these products should seek alternative treatments. According to a preprint of a study published on Wednesday, Lilly scientists tested several versions of compounded tirzepatide combined with various vitamin B12 analogs, which were on sale in the US. The analyses pinpointed a “widespread and previously unidentified” molecule in compounded tirzepatide/B12 products, resulting from a chemical reaction between tirzepatide and certain B12 analogs. Mass spectrometry analysis showed that the molecule is larger than tirzepatide, suggesting that it might consist of a B12 molecule bonded to tirzepatide, the researchers wrote. As well as finding the impurity, the tests showed “structural perturbations” in the tirzepatide in the samples, which could change the drug’s efficacy or pharmacologic profile. The scientists wrote that they were unaware of any studies, in humans or otherwise, evaluating the safety of the unidentified molecule. “Without such data, the impact of the impurity on efficacy, toxicity, and long‑term outcomes for patients taking these compounded combination drugs is unknown and may be substantial,” they wrote. They cited research from IQVIA stating that 80% of compounded weight loss drugs were combinations of tirzepatide or semaglutide — the active ingredient in Novo Nordisk’s Ozempic and Wegovy, among others — with sub-therapeutic amounts of B vitamins or other amino acids. Adding compounds like vitamin B12 to weight loss drugs allows compounders to claim they are providing “personalized” products and legally sidestep the drugs’ patent protection. In its letter, Lilly said that compounders have added other molecules to tirzepatide, including glycine, pyridoxine, niacinamide and carnitine. These add no proven benefit but introduce new risks, the company said. The study write-up has not yet undergone peer review. Lilly said that the compounders making these combination products were not required to monitor patients for side effects or to report any adverse events. Lilly has told the FDA about its findings. Last month, FDA chief Marty Makary said the agency would “take swift action against companies mass-marketing illegal copycat drugs.” This was backed up the following day with an announcement that the FDA would consider legal action, including seizure and injunction, against GLP-1 compounders who break the rules. Novo has recently taken a more conciliatory approach to this problem, reaching a truce with the compounder Hims & Hers. Novo had earlier sued Hims, whose off-brand versions of Novo drugs — including Ozempic and both the injected and pill forms of Wegovy — had been cutting into its sales in a major way.

Patent Infringement

12 Mar 2026

·firstwordpharma.com

Lilly warns of impurity in compounded versions of tirzepatide

Eli Lilly warned Thursday that combining tirzepatide with B12 — as offered by compounders in the US — can lead to the formation of an impurity caused by a chemical reaction between the dual GLP-1/GIP agonist and the additive. According to the company, "nothing is known" about the impurity's short- or long-term effects in humans, as tirzepatide has never been studied together with B12.Tirzepatide is approved in the US as Zepbound for treating obesity and moderate-to-severe obstructive sleep apnoea, and sold as Mounjaro for type 2 diabetes.The impurity was identified after Lilly tested 10 compounded products being marketed in the US that contain tirzepatide combined with B12, sometimes referred to as methylcobalamin, hydroxocobalamin or cyanocobalamin. The testing uncovered "significant levels" of the impurity. Unknown risksLilly said the risks to patients are unclear as the compounders making these combination drugs are not required to monitor or report adverse events. The company added that nothing is currently known about the impurity's potential impact on tirzepatide’s interaction with the GLP-1 and GIP receptors, toxicity, immune reactions, or how it is absorbed, distributed, metabolised and eliminated. "FDA warns that compounded products can be risky for patients because they are not reviewed for safety, effectiveness or quality. Adding a reactive substance like vitamin B12 without clinical testing or FDA review introduces additional unknown risks," said David Hyman, Lilly's chief medical officer.Although the FDA and a federal court have confirmed that mass-compounding of tirzepatide must stop, some firms are continuing the practice, claiming to offer "personalised" versions by adding additives, such as B12, glycine, pyridoxine, niacinamide or carnitine.Earlier this month, the FDA stepped up its efforts to combat misleading advertisements for compounded products, with the agency issuing warning letters to 30 telehealth firms for making false claims about their GLP-1 offerings. Lilly said Thursday that it has notified the regulator of its latest findings.Meanwhile, the pressure on telehealth firm Hims & Hers Health to stop advertising compounded versions of GLP-1 agonists appears to have paid off. Having quickly backtracked last month on plans to sell a compounded version of Novo Nordisk's oral Wegovy (semaglutide), the firm will now scale back its compounded offerings, in return for agreeing to sell the Danish company's GLP-1 medications and escaping a patent infringement lawsuit. For related analysis, see — Vital Signs: Hims finally feels the pressure on compounded GLP-1s, but leaves its options open.

Patent InfringementBiosimilarDrug Approval

01 Jul 2025

·www.prnewswire.com

NEW STUDY SHOWS SNACKING ON MIXED TREE NUTS MAY IMPACT CARDIOVASCULAR RISK FACTOR TMAO

New Findings Published in Nutrients in Partnership with the International Tree Nut Council Nutrition Research & Education Foundation DAVIS, Calif., July 1, 2025 /PRNewswire/ -- In a paper1 published online this week in the journal, Nutrients, researchers found that consuming mixed tree nuts (almonds, Brazil nuts, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts) in a hypocaloric diet resulted in reduced body weight and plasma levels of the cardiovascular risk factor trimethylamine N-oxide (TMAO). The decrease in TMAO levels was greatest among individuals with lower-quality baseline diets. In a previous study2, researchers at UCLA demonstrated that consuming 1.5 ounces of tree nuts per day (versus pretzels) during 24 weeks of weight loss and weight maintenance, resulted in weight loss, and decreased blood pressure and heart rate—signs of reduced cardiovascular risk. TMAO, a gut microbiome metabolite, is a novel cardiovascular disease risk factor. It is produced by the liver from trimethylamine (TMA), which is generated by gut bacteria from dietary precursors such as choline, phosphatidylcholine and L-carnitine. Diet can impact TMAO levels by modifying the gut microbiota, effecting the production of TMA from nutrients like choline and L-carnitine. Tree nuts, which are rich in phytochemicals such as carotenoids, phenolic acids and phytosterols, may also affect TMAO production. The current study looked at whether tree nut snacks, as part of a hypocaloric diet, could influence TMAO levels and their relationship with the gut microbiome. Plasma samples were collected and evaluated from 95 overweight or obese participants. Nutritional data were collected at baseline and week 12 via dietary recall. Each study participant was given a Healthy Eating Index (HEI) score, which is used to assess diet quality based on the Dietary Guidelines or Americans. According to lead researcher, Zhaoping Li, MD, PhD, Professor of Medicine and Chief of the Division of Clinical Nutrition at UCLA, "While the hypocaloric diet with tree nuts and pretzels both resulted in a significant reduction in plasma TMAO levels, the reduction of TMAO was more profound in those consuming mixed tree nuts with poor dietary habits and low HEI scores." Interestingly, the dietary intervention did not significantly alter the intake of dietary sources of TMAO, including choline and phosphatidylcholine. Therefore, the observed decrease in TMAO plasma levels is unlikely due to a reduction in TMAO precursors. "Adding mixed tree nuts to hypocaloric diets may not only help in the reduction of plasma TMAO levels, but may be an important intervention for managing cardiovascular health," stated Dr. Li. In support of these findings, Maureen Ternus, M.S., R.D., Executive Director of the International Tree Nut Council Nutrition Research & Education Foundation (INC NREF), emphasized, "This study is yet another piece of evidence showing that people should include more nuts in their diet. Just a handful of tree nuts (1.5 ounces or 1/3 cup) every day can result in numerous health benefits." The International Tree Nut Council Nutrition Research & Education Foundation (INC NREF) is a non-profit, non-governmental organization dedicated to supporting nutrition research and education for consumers and health professionals throughout the world. Members include those associations and organizations that represent the nine tree nuts (almonds, Brazils, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts). For more information, please visit our website at . 1 Lei, O., J. Yang, H.H. Kang, Z. Li., 2025. Impact of a 12-week hypocaloric weight loss diet with mixed tree nuts vs. pretzels on trimethylamine-n-oxide (TMAO) levels in overweight adults. Nutrients 17(13): 2137. 2 Wang, J., S. Wang, S.M., Henning, T. Qin, Y. Pan, J. Yang, J. Huang, C.-H. Tseng, D. Heber, Z. Li., 2021 Mixed tree nut snacks compared to refined carbohydrate snacks resulted in weight loss and increased satiety during both weight loss and weight maintenance: a 24-week randomized controlled trial. Nutrients. 13(5), 1512. SOURCE International Tree Nut Council Nutrition Research & Education Foundation WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical Result

100 Deals associated with Levocarnitine

External Link

KEGG	Wiki	ATC	Drug Bank
D02176	Levocarnitine	A16AA01	DB00583

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Kidney Diseases	Italy	Alfasigma SpA	18 May 2015
Shock, Septic	Italy	Alfasigma SpA	18 May 2015
Cardiovascular Diseases	China	Leadiant Biosciences, Inc.	31 Dec 1999
Metabolism, Inborn Errors	Ireland	Shire Pharmaceutical Development Ltd.	23 Oct 1996
Carnitine palmitoyltransferase deficiency	Netherlands	Sigma-Tau Industrie Farmaceutiche Riunite SpA	03 Feb 1986
Systemic Carnitine Deficiency	United States	Leadiant Biosciences, Inc.	27 Dec 1985

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Inflammation	Phase 3	Egypt	Tanta University	05 Mar 2023
Pain	Phase 3	Egypt	Tanta University	05 Mar 2023
Rheumatoid Arthritis	Phase 3	Egypt	Tanta University	05 Mar 2023
Moderate persistent asthma	Phase 3	Egypt	Tanta University	08 Aug 2022
Persistent asthma	Phase 3	Egypt	Tanta University	08 Aug 2022
Beta-Thalassemia	Phase 3	Egypt	Tanta University	08 Jul 2022
Refractory heart failure	Phase 3	China	Lee's Pharmaceutical Holdings Ltd.	01 Jan 2011
Nephrotoxicity	Phase 2	Egypt	Tanta University	10 Aug 2025
HMN (Hereditary Motor Neuropathy) Proximal Type I	Phase 2	United States	Leadiant Biosciences, Inc.	01 Apr 2008
HMN (Hereditary Motor Neuropathy) Proximal Type I	Phase 2	Canada	Leadiant Biosciences, Inc.	01 Apr 2008

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05083637 (Pubmed \| J Nutr)	Not Applicable	Malnutrition Myeloperoxidase \| Neopterin \| alpha-1-antitrypsin ... View more	98	L-carnitine syrup (100 mg/kg/d)	fxukapjfbb(uvzskhyhtr) = tncvuykllm kpixtdptyg (wnoglifguj, -556.58 to 249.91)	Negative	01 Mar 2024
NCT01783041 (CTgov)	Phase 2/3	Systemic Carnitine Deficiency \| Obstetric Labor, Premature \| Neurodevelopmental Disorders	144	5% Dextrose (5% Dextrose)	jtbcuvzxao(pwmouxsagk) = whcfzarnmc ywentaqwuk (tuafqctxdw, 3.5) View more	-	08 Mar 2022
				L-carnitine (L-carnitine)	jtbcuvzxao(pwmouxsagk) = urainbwttk ywentaqwuk (tuafqctxdw, 3.3) View more
NCT03426722 (Pubmed \| Invest New Drugs)	Phase 3	Gastrointestinal Stromal Tumors First line	42	L-carnitine	glstrimbio(dvjerdbnyw) = vicousaqqf mjvehsmfrh (hwhwhkjhel ) View more	-	01 Apr 2020
NCT01665092 (RACE, CTgov)	Phase 2	Shock, Septic	250	placebo (Control)	typogygsux(jwlsioaxgg) = sfpxyxaeky nrfgufptlt (ejfowuczgv, 0.35) View more	-	04 Jun 2019
				Levo-Carnitine (Carnitine Low)	typogygsux(jwlsioaxgg) = pwrvuynupa nrfgufptlt (ejfowuczgv, 0.66) View more
NCT05817799 (Pubmed \| Eur J Clin Nutr)	Phase 2/3	-	91	L-carnitine supplementation	ahgfhozkqy(jflfngghqm): P-Value = 0.0007 View more	Positive	01 Feb 2019
				L-carnitine (No injections)
NCT01665092 (RACE, Pubmed \| JAMA Netw Open)	Phase 2	Shock, Septic	250	Levocarnitine 18g	lvnyqqxjlf(jvplswsquh) = fxogwbkqjh qyolkhioaq (bmqommchzj )	Negative	07 Dec 2018
				Placebo	lvnyqqxjlf(jvplswsquh) = hxopmclnxg qyolkhioaq (bmqommchzj )
NCT00754767 (CTgov)	Phase 4	Drug intoxication \| Neurotoxicity Syndromes \| Metastatic breast cancer ... View more	2	L-Carnitine (Arm I L-Carnitine)	oyhczvgfse(drlusxdlcv) = kevevrfous syusaloyci (rlwtbhkqxz, rgjnfjcwgj - okybozlyum) View more	-	13 Apr 2017
				placebo (Arm II-Placebo)	oyhczvgfse(drlusxdlcv) = jtmrgehwwa syusaloyci (rlwtbhkqxz, lpcnjomaib - ohugmfvlrk) View more
NCT00661453 (CTgov)	Phase 1/2	HMN (Hereditary Motor Neuropathy) Proximal Type I	40	carnitine+Valproic Acid	npgrobivek(jktcvecorh) = iboucxgwce waojuphszb (zjgtutqltw, 1334.48) View more	-	15 Jun 2015
NCT01107730 (CTgov)	Phase 3	Atrial Fibrillation	33	L-Carnitine (L-Carnitine)	qagueocdnm = wvhpqosnkw kzkgdapzbd (mjdolaazxi, suqvrkmenp - dnhiuozfam) View more	-	13 May 2015
				Vitamin C (Vitamin C)	qagueocdnm = lvxlqkhrgw kzkgdapzbd (mjdolaazxi, bironmbbnu - wsialygvti) View more
NCT00227266 (SMA CARNI-VAL Trial, CTgov)	Phase 2	Spinal Muscular Atrophy \| Juvenile Spinal Muscular Atrophy \| Muscular Atrophy, Spinal, Type II	94	Placebo (Cohort 1a Sitters Placebo Then Treatment)	cmoaxofygb(bnotfxoizo) = mqctahtweq rqnebokkzs (rakfnudbmx, 9.3) View more	-	03 May 2011
				Carnitor+VPA (Cohort 1b Sitters Treatment)	cmoaxofygb(bnotfxoizo) = hvraxbukur rqnebokkzs (rakfnudbmx, 8.7) View more

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