The molecular mechanism of glutamine inhibiting Drp1/FUNDC1 activation and reversing inflammation-induced mitophagy in amniotic epithelial cells to prevent and treat premature rupture of membranes in pre-preterm rupture of fetal membranes

Start Date23 Jan 2025

Sponsor / Collaborator-

IRCT20230626058586N6

/ SuspendedNot ApplicableIIT

Investigating the effect of glutamine supplementation on the Rectus Femoris and Vastus Intermedius mascles thinckness in patients undergoing laparoscopic sleeve gastrectomy

Start Date20 Jan 2025

Sponsor / Collaborator

Shahid Beheshti University of Medical Sciences

IRCT20200929048876N4

/ RecruitingNot ApplicableIIT

Evaluation the effect of glutamine on inflammation and infectious events in patients with mild burns involving under 20% of the body area

Start Date21 Oct 2024

Sponsor / Collaborator

Zanjan University of Medical Sciences

100 Clinical Results associated with L-Glutamine

100 Translational Medicine associated with L-Glutamine

100 Patents (Medical) associated with L-Glutamine

66,615

Literatures (Medical) associated with L-Glutamine

01 Dec 2025·MOLECULAR BIOLOGY REPORTS

Two different complement Factor B (Bf) alleles of the orangutan major histocompatibility complex (MHC) are also conserved in chimpanzee and humans showing importance in primate immunity

Article

Author: Lledo, Tomás ; Juarez, Ignacio ; Martín-Villa, José Manuel ; Arnaiz-Villena, Antonio ; Vaquero-Yuste, Christian ; Suarez-Trujillo, Fabio

BACKGROUND:

Major Human Histocompatibility complex (MHC or HLA in humans) has been associated to autoimmune diseases. However, only statistical phenomenological and no pathogenetic description has been reached after decades. This shows that MHC single locus association studies are probably useless for HLA/diseases association. Extended HLA (class I and class II genes) haplotypes should also be studied conjointly with class III or complement alleles (complotypes). Complotypes in humans are defined as alleles belonging to C2, C4 and Bf (Factor B) genes/proteins (class III). Also, the placing of MHC class I and class II genes close together with complement genes from at least birds to humans shows existence of a strong selection to gather conjointly these loci that fight microbes, help self-maintenance and avoid autoimmunity. In this paper we aim to study Bf alleles in primates in order to rise again interest to study the role of Bf alleles together with other MHC genes in their physiopathology and evolution.

METHODS:

Orangutan (Pongo pygmaeus, Popy) cell lines RNA from 6 different individuals were retrotranscribed, PCR amplified, cloned and DNA sequenced in order to study Bf alleles.

RESULTS:

A Bf allele identical to that found in chimpanzee (Patr-Bf*A01) and human (rs641153) was found in two of the six studied orangutans: Popy-Bf*A01 and Popy-Bf*A02. This polymorphism is placed in Factor B codon 32 that defines BF*S and Bf*F proteins in man and produce Leu instead of Arg (Bf*S) or Gln (Bf*F). In addition, each new orangutan allele present synonymous differences with each other at codon 25: Popy-Bf*A01 shows ACG while Popy-Bf*A02 bears ACA, both codifying for Thr.

CONCLUSIONS:

The selection for about 15 million years (time gap of evolutionary appearance between orangutan and hominids) shows the importance of this particular allele conservation in immune and self defense in primates. The complotypes (Bf,C2 and C4 loci) alleles together with other MHC class I and Cass II loci alleles are often transmitted in block to the germinal line: this indicates that all specific alleles from the MHC different loci may work together to accomplish MHC functions. All MHC loci alleles should be studied together to unveil their physiopathology and also maintenance of specific alleles (like the one described in this paper) for so long time in evolution should be further studied in Bf and the other neighbouring complement loci (C2 and C4).

01 Sep 2025·Neural Regeneration Research

Targeting harmful effects of non-excitatory amino acids as an alternative therapeutic strategy to reduce ischemic damage

Article

Author: Kirov, Sergei A. ; Carretero, Victoria Jiménez ; Hernández-Campano, Jorge ; Álvarez-Merz, Iris ; Hernández-Guijo, Jesús M.

The involvement of the excitatory amino acids glutamate and aspartate in cerebral ischemia and excitotoxicity is well-documented. Nevertheless, the role of non-excitatory amino acids in brain damage following a stroke or brain trauma remains largely understudied. The release of amino acids by necrotic cells in the ischemic core may contribute to the expansion of the penumbra. Our findings indicated that the reversible loss of field excitatory postsynaptic potentials caused by transient hypoxia became irreversible when exposed to a mixture of just four non-excitatory amino acids (L-alanine, glycine, L-glutamine, and L-serine) at their plasma concentrations. These amino acids induce swelling in the somas of neurons and astrocytes during hypoxia, along with permanent dendritic damage mediated by N-methyl-D-aspartate receptors. Blocking N-methyl-D-aspartate receptors prevented neuronal damage in the presence of these amino acids during hypoxia. It is likely that astroglial swelling caused by the accumulation of these amino acids via the alanine-serine-cysteine transporter 2 exchanger and system N transporters activates volume-regulated anion channels, leading to the release of excitotoxins and subsequent neuronal damage through N-methyl-D-aspartate receptor activation. Thus, previously unrecognized mechanisms involving non-excitatory amino acids may contribute to the progression and expansion of brain injury in neurological emergencies such as stroke and traumatic brain injury. Understanding these pathways could highlight new therapeutic targets to mitigate brain injury.

01 May 2025·JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY A-CHEMISTRY

Two birds with one stone: A near-infrared AIE fluorescent probe for highly selective recognition of Cu2+/GSH and bioimaging

Author: Wang, Shizhen ; Miao, Hui ; Zhang, Yuanqian ; Song, Qixiang ; Xue, Wenhui ; Wei, Biao ; Qiao, Rui ; Dong, Yajie ; Hu, Jingde ; Wang, Xin ; Qu, Changqing ; Chen, Mengyu ; Bai, Cuibing

Although notable progress has been made in the identification of Cu²⁺ and glutathione (GSH), probes that can specifically recognize them simultaneously are still rare.Herein, we designed, synthesized, and characterized a fluorescent probe QA with aggregation-induced emission characteristics, a near-IR emission wavelength (688 nm), a large Stokes shift (Δλ = 263 nm), and specific sequential recognition of Cu²⁺ and GSH.Compared with other probes, QA exhibits a fast fluorescence "ON-OFF" response to Cu²⁺, and its low limit of detection (LOD) toward Cu²⁺ is 3.53 x 10^-8 M.Moreover, it can also detect Cu²⁺ in actual water samples.Moreover, QA-Cu²⁺ shows high sensitivity to GSH with an LOD of 3.47 x 10^-7 M.Notably, the toxicity of QA is so low that it can recognize Cu²⁺ and GSH in various models, including HepG-2 cells, Caenorhabditis elegans, and adult mice, implying that it is a favorable applicant to detect Cu²⁺ and GSH in vitro and in vivo.

News (Medical) associated with L-Glutamine

25 Oct 2024

·www.prnewswire.com

KIND Announces FDA Granted Orphan Drug Designation (ODD) for AND017 in the Treatment of Sickle Cell Disease (SCD)

SAN FRANCISCO, Oct. 25, 2024 /PRNewswire/ -- Kind Pharmaceutical ("Hangzhou Andao Pharmaceutical Ltd. and Kind Pharmaceuticals LLC"), a clinical-stage biopharmaceutical company focused on developing innovative medicines to treat hematological diseases and cancers, today announced that the U.S. Food and Drug Administration (FDA) Office of Orphan Products Development has granted Orphan Drug Designation (ODD) to AND017 in the treatment of Sickle Cell Disease (SCD). AND017 is being developed to treat various anemia indications associated with diseases including non-dialysis dependent chronic kidney disease (NDD-CKD) and dialysis-dependent chronic kidney disease (DD-CKD). The results for AND017's phase 1 in healthy subjects and phase 2 clinical trials in treatment of anemia in NDD-CKD and anemia in DD-CKD are currently being presented at the annual meeting of American Society of Nephrology (ASN) Kidney Week in San Diego. The preclinical work supporting AND017's ODD in SCD will be presented in future scientific meeting and subsequently published in a scientific journal. Sickle Cell Disease (SCD) is a devasting genetic disease with US patient population around 120,000; SCD disproportionally affects Black and African Americans, comprising more than 98% of patients living with this disease. "The FDA's granting of ODD for AND017 underscores the urgent medical need for new therapies, particularly oral drugs to safely and effectively treat patients with SCD," said Dong Liu, Ph.D., Founder, Chairman, and CEO of Kind Pharmaceutical. "The granting of ODD also demonstrates the innovation capability and the vision of Kind Pharmaceutical." "Hydroxyurea and L-glutamine are the limited FDA-approved oral treatments for SCD, AND017 from Kind Pharmaceutical might not only provide a novel oral treatment with unique mechanism of action, but also an obvious better safety and efficacy profile." said Prof. Gang Huang at UT Health San Antonio, Kathryn Mays Johnson Distinguished Chair in Oncology, who is an expert in studies of hematology and various blood diseases, and involved in the preclinical studies of AND017 in SCD. "I am eager to see how a compound with such unbelievable preclinical safety and efficacy data will translate to real world SCD patients." FDA Orphan Drug Designation (ODD) is granted to a drug or biological product to prevent, diagnose or treat a rare disease or condition that affects fewer than 200,000 people in the United States. ODD qualifies KIND for incentives including tax credit for qualified clinical trials, exemption from user fees, and potential seven years of market exclusivity after AND017's approval for treatment of Sickle Cell Disease (SCD). About Sickle Cell Disease (SCD) Sickle Cell Disease (SCD) affects around 120,000 patients in US and more than 8,000,000 worldwide. As a genetic disease with a single amino acid mutation in the β-globin of mature adult hemoglobin, the hemoglobin molecules of in the red blood cells (RBCs) of SCD patients are prone to aggregate in the tissue after the dissociation of oxygen molecules, which would cause the RBCs sickling in the blood stream and eventually lead to hemolysis and occlusion of capillaries; therefore the hallmarks of SCD are hemolytic anemia and vaso-occlusive crises (VOCs); and SCD causes multiorgan failure and premature death. About AND017 AND017 is a first-in-class hemoglobin elevating agent (HbEA) that targets multiple stages of the red blood cell (RBC) life cycle and is being developed to treat anemia associated with dialysis-dependent chronic kidney disease (DD-CKD), non-dialysis dependent chronic kidney disease (NDD-CKD), cancer-related anemia (CRA), myelodysplastic syndromes (MDS) anemia, sickle cell disease (SCD), and β-thalassemia. About Kind Pharmaceutical ("Hangzhou Andao Pharmaceutical Ltd. and Kind Pharmaceuticals LLC") KIND is a clinical-stage biopharmaceutical company focused on developing innovative medicines to treat hematological diseases and cancers. The company's mission, "kind to human, humble to science, good to patients", drives its commitment to advancing current science to meet unmet medical need. KIND's lead clinical candidate, AND017, first-in-class hemoglobin elevating agent (HbEA), is being developed for treating anemia of various disorders, including dialysis dependent chronic kidney disease (DD-CKD) associated anemia, non-dialysis dependent (NDD) CKD associated anemia, cancer related anemia (CRA), myelodysplastic syndromes (MDS) anemia, sickle cell disease (SCD), and β-thalassemia. KIND's second clinical candidate, AND019, an orally available brain penetrant selective estrogen receptor degrader (SERD), is being developed to treat ER+/Her2- breast cancer. KIND is also developing promising disruptive next generation ADC technologies. For details, please visit . Contact: Dong Liu, PhD, Chairman and CEO of Kind Pharmaceutical Email: [email protected] Tel: 650-315 6151 SOURCE KInd Pharmaceuticals WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical ResultOrphan DrugPhase 2

25 Oct 2024

·www.biospace.com

KIND Announces FDA Granted Orphan Drug Designation (ODD) for AND017 in the Treatment of Sickle Cell Disease (SCD)

SAN FRANCISCO , Oct. 25, 2024 /PRNewswire/ -- Kind Pharmaceutical (“Hangzhou Andao Pharmaceutical Ltd. and Kind Pharmaceuticals LLC”), a clinical-stage biopharmaceutical company focused on developing innovative medicines to treat hematological diseases and cancers, today announced that the U.S. Food and Drug Administration (FDA) Office of Orphan Products Development has granted Orphan Drug Designation (ODD) to AND017 in the treatment of Sickle Cell Disease (SCD). AND017 is being developed to treat various anemia indications associated with diseases including non-dialysis dependent chronic kidney disease (NDD-CKD) and dialysis-dependent chronic kidney disease (DD-CKD). The results for AND017’s phase 1 in healthy subjects and phase 2 clinical trials in treatment of anemia in NDD-CKD and anemia in DD-CKD are currently being presented at the annual meeting of American Society of Nephrology (ASN) Kidney Week in San Diego . The preclinical work supporting AND017’s ODD in SCD will be presented in future scientific meeting and subsequently published in a scientific journal. Sickle Cell Disease (SCD) is a devasting genetic disease with US patient population around 120,000; SCD disproportionally affects Black and African Americans, comprising more than 98% of patients living with this disease. “The FDA’s granting of ODD for AND017 underscores the urgent medical need for new therapies, particularly oral drugs to safely and effectively treat patients with SCD,” said Dong Liu , Ph.D., Founder, Chairman, and CEO of Kind Pharmaceutical. “The granting of ODD also demonstrates the innovation capability and the vision of Kind Pharmaceutical.” “Hydroxyurea and L-glutamine are the limited FDA-approved oral treatments for SCD, AND017 from Kind Pharmaceutical might not only provide a novel oral treatment with unique mechanism of action, but also an obvious better safety and efficacy profile.” said Prof. Gang Huang at UT Health San Antonio, Kathryn Mays Johnson Distinguished Chair in Oncology, who is an expert in studies of hematology and various blood diseases, and involved in the preclinical studies of AND017 in SCD. “I am eager to see how a compound with such unbelievable preclinical safety and efficacy data will translate to real world SCD patients.” FDA Orphan Drug Designation (ODD) is granted to a drug or biological product to prevent, diagnose or treat a rare disease or condition that affects fewer than 200,000 people in the United States . ODD qualifies KIND for incentives including tax credit for qualified clinical trials, exemption from user fees, and potential seven years of market exclusivity after AND017’s approval for treatment of Sickle Cell Disease (SCD). About Sickle Cell Disease (SCD) Sickle Cell Disease (SCD) affects around 120,000 patients in US and more than 8,000,000 worldwide. As a genetic disease with a single amino acid mutation in the β-globin of mature adult hemoglobin, the hemoglobin molecules of in the red blood cells (RBCs) of SCD patients are prone to aggregate in the tissue after the dissociation of oxygen molecules, which would cause the RBCs sickling in the blood stream and eventually lead to hemolysis and occlusion of capillaries; therefore the hallmarks of SCD are hemolytic anemia and vaso-occlusive crises (VOCs); and SCD causes multiorgan failure and premature death. About AND017 AND017 is a first-in-class hemoglobin elevating agent (HbEA) that targets multiple stages of the red blood cell (RBC) life cycle and is being developed to treat anemia associated with dialysis-dependent chronic kidney disease (DD-CKD), non-dialysis dependent chronic kidney disease (NDD-CKD), cancer-related anemia (CRA), myelodysplastic syndromes (MDS) anemia, sickle cell disease (SCD), and β-thalassemia. About Kind Pharmaceutical (“Hangzhou Andao Pharmaceutical Ltd. and Kind Pharmaceuticals LLC”) KIND is a clinical-stage biopharmaceutical company focused on developing innovative medicines to treat hematological diseases and cancers. The company’s mission, “kind to human, humble to science, good to patients”, drives its commitment to advancing current science to meet unmet medical need. KIND’s lead clinical candidate, AND017, first-in-class hemoglobin elevating agent (HbEA), is being developed for treating anemia of various disorders, including dialysis dependent chronic kidney disease (DD-CKD) associated anemia, non-dialysis dependent (NDD) CKD associated anemia, cancer related anemia (CRA), myelodysplastic syndromes (MDS) anemia, sickle cell disease (SCD), and β-thalassemia. KIND’s second clinical candidate, AND019, an orally available brain penetrant selective estrogen receptor degrader (SERD), is being developed to treat ER+/Her2- breast cancer. KIND is also developing promising disruptive next generation ADC technologies. For details, please visit . Contact: Dong Liu , PhD, Chairman and CEO of Kind Pharmaceutical Email: liudong@kindpharmaceutical.com Tel: 650-315 6151 View original content: SOURCE KInd Pharmaceuticals

Clinical ResultOrphan DrugPhase 2

26 Sep 2024

·www.outsourcing-pharma.com

Pfizer withdraws sickle cell disease drug Oxbryta amid safety concerns

The withdrawal decision was prompted by clinical data indicating that the overall benefit of Oxbryta “no longer outweighs the risk” in its target patient population, the company said in a public release . Specifically, the trials outline an “imbalance” in vaso-occlusive crises and fatal events that the company will assess further. The move to stop clinical trials of the drug will last while Pfizer further reviews the available data and investigates the findings. Sickle cell disease is a genetic blood disorder where patients have a mutation in hemoglobin, a protein found in red blood cells. This leads the protein to clump together, causing cells to have a sickle shape that can block blood vessels and carry less oxygen, leading to acute pain and anemia. Oxbryta, whose generic name is voxelotor, is an oral small molecule drug that was first approved by the US Food and Drug Administration (FDA) for the treatment of sickle cell disease in 2019, with an EU approval granted in 2022. The drug is designed to make hemoglobin better at carrying oxygen and less prone to clumping together, making red blood cells more functional. The treatment was previously developed by the U.S. firm Global Blood Therapeutics before the company was snapped up by Pfizer for $5.4 billion in 2022 , and bagged Pfizer $328 million in revenues in 2023 . The big pharma company has notified regulators about the data and doesn’t expect the event to impact its full-year 2024 financial guidance. Nevertheless, the company’s stock price on the New York Stock Exchange slumped by more than 1% at the news yesterday (Wednesday 25th September). googletag.cmd.push(function () { googletag.display('text-ad1'); }); Emphasizing Pfizer’s focus on patient safety, chief medical officer and head of worldwide medical and safety, Aida Habtezion, said in the company release that the Pfizer’s “primary concern is for patients who suffer from SCD, which remains a very serious and difficult-to-treat disease with limited treatment options. We advise patients to contact their physicians to discuss alternative treatment while we continue to investigate the findings from our review of the data.” The global market for sickle cell disease was worth $2.25 billion in 2022 and is expected to grow by 20.1% per year to $9.84 billion by 2030. The main players in the market have included Pfizer with Oxbryta, Novartis with the antibody Adakveo (crizanlizumab) and Generex Biotechnology’s Emmaus Medical with Endari (L-glutamine). In 2017, Endari became the first branded drug for sickle cell disease in decades when it was greenlit by the U.S. FDA. Another driver for the sickle cell disease market is gene therapy, with the first cell-based gene therapies – Casgevy by Vertex Pharmaceuticals and Lyfgenia by Bluebird Bio – approved by the U.S. FDA in late 2023 .

Drug ApprovalGene Therapy

100 Deals associated with L-Glutamine

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KEGG	Wiki	ATC	Drug Bank
D00015	L-Glutamine	A16AA03	DB00130

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Indication	Country/Location	Organization	Date
Anemia, Sickle Cell	US	Emmaus Medical, Inc.	07 Jul 2017
Short Bowel Syndrome	US	Emmaus Medical, Inc.	10 Jun 2004

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Indication	Highest Phase	Country/Location	Organization	Date
Beta-Thalassemia	Phase 3	US	Emmaus Medical, Inc.	01 May 2010
Gastrointestinal Neoplasms	Phase 3	FR	Nestlé SA	01 Oct 2007
Diverticulitis	Phase 2	US	Emmaus Medical, Inc.	31 Oct 2021
Cystic Fibrosis	Phase 2	US	Emmaus Medical, Inc.	01 Feb 2010
Pancreatic Ductal Adenocarcinoma	Phase 1	US	Emmaus Medical, Inc.	13 May 2021
Diverticulosis, Colonic	Phase 1	US	Emmaus Medical, Inc.	19 Jul 2019
Diverticulosis, Esophageal	Phase 1	US	Emmaus Medical, Inc.	19 Jul 2019
Diabetes Mellitus, Type 2	Phase 1	US	Emmaus Medical, Inc.	24 Jun 2019
Sepsis	Preclinical	CN	Third Military Medical University	20 Dec 2022

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01952847 (CTgov)	Phase 3	Neoplasms \| Mucositis \| Stomatitis ... View more	77	Questionnaires+Glutamine (Radiation Therapy to Esophagus Patient Group - Glutamine)	bbpkwkfllv(qlxyvmoxvy) = veljapjequ dgujyvdwku (qtavrxcfpw, wjvaqdevlx - ihaonioovf) View more	-	15 Jun 2022
				Questionnaires (Radiation Therapy to Esophagus Patient Group - Placebo)	bbpkwkfllv(qlxyvmoxvy) = rhcbcmnyge dgujyvdwku (qtavrxcfpw, srhkrhscvq - btoynutuju) View more
EHA2022	Phase 3	Anemia, Sickle Cell	19	L-glutamine	yemkphxvur(ckdiwroybo) = zwgqyghaft cgjmtvdaom (knifakkifb ) View more	-	12 May 2022
NCT05054517 (Pubmed \| Oncol Lett)	Not Applicable	-	72	Patients receiving oral glutamine supplementation	qdszbsaops(xopmpdjdax) = dshanexsgk tlsxppokuk (ipqenemiac ) View more	-	01 Jan 2022
NCT01048905 (CTgov)	Phase 2	Thalassemia \| Associated Pulmonary Arterial Hypertension \| Anemia, Sickle Cell	13	L-Glutamine	mlskgsrqon(kzridtexbr) = foskjyqvjn zojicawvgx (atnqeesikn, zbnlkvdxzs - edoszxzspz) View more	-	10 Jun 2021
NCT01952847 (Pubmed \| Invest New Drugs)	Phase 3	Radiation esophagitis	53	Glutamine	mvgjtvuwdm(cisdekzmwz) = podmjkwqka rgsdcuejkn (tmyohbzneu ) View more	Negative	13 Feb 2021
				Glycine placebo	mvgjtvuwdm(cisdekzmwz) = hcrtttmkts rgsdcuejkn (tmyohbzneu ) View more
NCT00586209 (CTgov)	Phase 2	Thalassemia \| Anemia, Sickle Cell	15	L-Glutamine (L-glutamine)	gjhqhsmojp(juxwhogxak) = yqjfrjfawo qnaucgwsou (ttzpkuwimy, yrmuanjkmf - rlvngzitus) View more	-	02 Feb 2021
				Placebo (Placebo)	gjhqhsmojp(juxwhogxak) = tadjqxkhda qnaucgwsou (ttzpkuwimy, lrywnwxbmu - klathvyual) View more
NCT00125788 (CTgov)	Phase 2	Thalassemia \| Anemia, Sickle Cell	70	L-glutamine (Investigational Product)	jpqjumrfll(mzqfgbtosk) = hrqmubwnok iiefjuhimw (hoksfdewnh, hzferwzujb - azrmvwlczy) View more	-	29 Jan 2021
				Placebo (Placebo)	jpqjumrfll(mzqfgbtosk) = izvrbrqjdi iiefjuhimw (hoksfdewnh, jvfhvihibj - mvyylxveqf) View more
NCT01534663 (GLUTFISH-HF, CTgov)	Phase 2/3	Hydrops Fetalis \| Heart Failure	31	Placebo (Placebo)	lvchtrtcoa(mtrjlgsuuv) = uhzgwytqxs memftlvtpf (qpxayqlnie, gzqwwuxfkx - uuumegcqwm) View more	-	22 Dec 2020
				Glutamine (Glutamine/Fishoil)	lvchtrtcoa(mtrjlgsuuv) = wsqqjphrkx memftlvtpf (qpxayqlnie, hduxjcrbdc - bynxhcgtqc) View more
NCT01783522 (CTgov)	Phase 2	Drug intoxication \| Multiple Myeloma \| Peripheral Nervous System Diseases	9	quality-of-life assessment+glutamine (Arm I (Preventative Nutritional Supplementation))	wjgwojjndj(jynerfgmya) = cccbgvggzs tkghrynkrx (sbhmmiizai, zqrlvvfwlr - zasmbtxbwk) View more	-	22 Oct 2019
				placebo (Arm II (Placebo))	wjgwojjndj(jynerfgmya) = aekuhxoluz tkghrynkrx (sbhmmiizai, dftfmlulxx - jcnxognzsd) View more
NCT02012608 (CTgov)	Phase 2	Breast Cancer	14	Glutamine (Glutamine)	aplptmxahe(geclwfmfif) = dcwconrkkn fhqtkpjqwv (kkxwyngxwf, ffrdlvwqhn - rcepbbskmr) View more	-	29 May 2019
				Placebo (Placebo)	aplptmxahe(geclwfmfif) = uckcifsfyw fhqtkpjqwv (kkxwyngxwf, uvtegaleft - cxvtvbjlsr) View more

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