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1. Full Text Lack of Therapeutic Effect of the Histone Deacetylase Inhibitor Vorinostat in Patients with Metastatic Radioiodine-Refractory Thyroid Carcinoma
by Woyach, Jennifer A and Kloos, Richard T and Ringel, Matthew D and Arbogast, Daria and Collamore, Minden and Zwiebel, James A and Grever, Michael and Villalona-Calero, Miguel and Shah, Manisha H
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 01/2009, Volume 94, Issue 1, pp. 164 - 170
Context: Aberrant histone deacetylase activity is seen in a variety of malignancies, and histone deacetylase inhibitors such as vorinostat have been shown to... 
SODIUM/IODIDE SYMPORTER | CANCER CELLS | SUBEROYLANILIDE HYDROXAMIC ACID | RADIOACTIVE IODINE THERAPY | ENDOCRINOLOGY & METABOLISM | MYELOID-LEUKEMIA | T-CELL LYMPHOMA | VALPROIC ACID | DEPSIPEPTIDE FR901228 | TRICHOSTATIN-A | SODIUM PHENYLBUTYRATE | Calcitonin - blood | Humans | Middle Aged | Carcinoma, Medullary - pathology | Male | Antineoplastic Agents - therapeutic use | Thyroid Neoplasms - radiotherapy | Carcinoembryonic Antigen - analysis | Enzyme Inhibitors - therapeutic use | Thyroglobulin - blood | Carcinoma, Medullary - drug therapy | Iodine Radioisotopes - therapeutic use | Neoplasm Metastasis | Thyroid Neoplasms - drug therapy | Adult | Female | Hydroxamic Acids - therapeutic use | Aged | Histone Deacetylase Inhibitors | Carcinoma, Medullary - radiotherapy | Thyroid Neoplasms - pathology | Index Medicus | Abridged Index Medicus | Original
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2. Full Text Placental endoplasmic reticulum stress in gestational diabetes: the potential for therapeutic intervention with chemical chaperones and antioxidants
by Yung, Hong-wa and Alnæs-Katjavivi, Patji and Jones, Carolyn J. P and El-Bacha, Tatiana and Golic, Michaela and Staff, Anne-Cathrine and Burton, Graham J
Diabetologia, ISSN 0012-186X, 10/2016, Volume 59, Issue 10, pp. 2240 - 2250
Aims/hypotheis The aim of this work was to determine whether placental endoplasmic reticulum (ER) stress may contribute to the pathophysiology of gestational... 
Antioxidants | Placenta | Trophoblast | Chaperones | Gestational diabetes | Metabolic acidosis | Endoplasmic reticulum stress | Unfolded protein response | CELLS | FETAL-GROWTH | ACIDOSIS | MELLITUS | PREGNANCY | INHIBITION | GROWTH-HORMONE | ENDOCRINOLOGY & METABOLISM | CAUSATION | Cell Line | Diabetes, Gestational - blood | Unfolded Protein Response - drug effects | Diabetes, Gestational - metabolism | Endoplasmic Reticulum Stress - drug effects | Acidosis - drug therapy | Humans | Glucose - pharmacology | Blotting, Western | Blood Glucose - drug effects | Placenta - metabolism | Pregnancy | Taurochenodeoxycholic Acid - pharmacology | Antioxidants - therapeutic use | Ascorbic Acid - pharmacology | Eukaryotic Initiation Factor-2 - metabolism | Phenylbutyrates - pharmacology | Adult | Female | Phosphorylation - drug effects | Endoplasmic Reticulum Stress - physiology | Vitamin E - pharmacology | Diet therapy | Physiological aspects | Aluminum compounds | Stress (Physiology) | Diabetes in pregnancy | Glucose | Glucose tolerance tests | Health aspects | Dextrose | Index Medicus
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3. Full Text Phase 1 and pharmacologic study of MS-275, a histone deacetylase inhibitor, in adults with refractory and relapsed acute leukemias
by Gojo, Ivana and Jiemjit, Anchalee and Trepel, Jane B and Sparreboom, Alex and Figg, William D and Rollins, Sandra and Tidwell, Michael L and Greer, Jacqueline and Eun, Joo Chung and Lee, Min-Jung and Gore, Steven D and Sausville, Edward A and Zwiebel, James and Karp, Judith E
Blood, ISSN 0006-4971, 04/2007, Volume 109, Issue 7, pp. 2781 - 2790
MS-275 is a benzamide derivative with potent histone deacetylase (HDAC) inhibitory and antitumor activity in preclinical models. We conducted a phase 1 trial... 
SUBEROYLANILIDE HYDROXAMIC ACID | BONE-MARROW-TRANSPLANTATION | CHRONIC LYMPHOCYTIC-LEUKEMIA | ACUTE MYELOID-LEUKEMIA | TRANS-RETINOIC ACID | SYNERGISTICALLY INDUCES APOPTOSIS | AGENT SODIUM PHENYLBUTYRATE | HEMATOLOGY | VIVO ANTITUMOR-ACTIVITY | MYELODYSPLASTIC SYNDROMES | ACUTE PROMYELOCYTIC LEUKEMIA | Benzamides - pharmacokinetics | Humans | Middle Aged | Pyridines - pharmacokinetics | Male | Antineoplastic Agents - therapeutic use | Leukemia - metabolism | Antineoplastic Agents - administration & dosage | Neoplasm Proteins - metabolism | Enzyme Inhibitors - administration & dosage | Benzamides - administration & dosage | Benzamides - therapeutic use | Enzyme Inhibitors - pharmacokinetics | Aged, 80 and over | Adult | Female | Antineoplastic Agents - pharmacokinetics | Acetylation | Pyridines - therapeutic use | Pyridines - administration & dosage | Leukemia - drug therapy | Enzyme Inhibitors - therapeutic use | Aged | Histone Deacetylase Inhibitors | Histones - metabolism | Index Medicus | Abridged Index Medicus | Clinical Trials and Observations
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4. Full Text A therapeutic strategy uses histone deacetylase inhibitors to modulate the expression of genes involved in the pathogenesis of rheumatoid arthritis
by Chung, Yih Lin and Lee, Ming Yuan and Wang, Ae June and Yao, Lin Fen
Molecular therapy : the journal of the American Society of Gene Therapy, ISSN 1525-0016, 11/2003, Volume 8, Issue 5, pp. 707 - 717
Rheumatoid arthritis (RA) is characterized by progressive destruction of the affected joints. The pathophysiology results from genetic susceptibility and... 
Immunohistochemistry | Tumor Necrosis Factor-alpha - metabolism | Leukocytes, Mononuclear - metabolism | Phenylbutyrates - therapeutic use | Cyclin-Dependent Kinase Inhibitor p21 | Rats, Long-Evans | Enzyme Inhibitors - pharmacology | Rats | Male | Blotting, Western | Gene Expression Regulation - drug effects | Animals | Cyclins - metabolism | Time Factors | Arthritis, Rheumatoid - drug therapy | Inflammation - drug therapy | Cell Division | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Hydroxamic Acids - therapeutic use | Histone Deacetylase Inhibitors | Acetylation | Histones - metabolism | Disease Models, Animal | Index Medicus
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5. Full Text Use of sodium 4-phenylbutyrate to define therapeutic parameters for reducing intracerebral hemorrhage and myopathy in Col4a1 mutant mice
by Hayashi, Genki and Labelle-Dumais, Cassandre and Gould, Douglas B
DMM Disease Models and Mechanisms, ISSN 1754-8403, 07/2018, Volume 11, Issue 7, p. dmm034157
Collagen type IV alpha 1 (COL4A1) and alpha 2 (COL4A2) form heterotrimers that constitute a major component of nearly all basement membranes. COL4A1 and COL4A2... 
Stroke | COL4A1 | Collagen | Chaperones | Drug therapy | Cerebral small vessel disease | Intracerebral hemorrhage | Myopathy | COLLAGEN-IV | PHENOTYPE | PATHOLOGY | CELL BIOLOGY | OCULAR DYSGENESIS | SMALL-VESSEL DISEASE | PATHOGENIC MECHANISMS | ANEURYSMS | CALCIFICATION | MUTATIONS | GENOME-WIDE ASSOCIATION | Animals, Newborn | Neuroprotective Agents - therapeutic use | Severity of Illness Index | Cerebral Hemorrhage - drug therapy | Phenylbutyrates - therapeutic use | Mice, Inbred C57BL | Male | Muscular Diseases - pathology | Cerebral Hemorrhage - genetics | Aging - pathology | Animals | Neuroprotective Agents - pharmacology | Time Factors | Mice, Mutant Strains | Muscular Diseases - drug therapy | Phenylbutyrates - administration & dosage | Collagen Type IV - genetics | Phenylbutyrates - pharmacology | Female | Muscular Diseases - genetics | Neuroprotective Agents - administration & dosage | Cerebral Hemorrhage - complications | Cerebral Hemorrhage - pathology | Physical Conditioning, Animal | Index Medicus
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6. Full Text Epigenetic therapy upregulates the tumor suppressor microRNA-126 and its host gene EGFL7 in human cancer cells
by Saito, Yoshimasa and Friedman, Jeffrey M and Chihara, Yoshitomo and Egger, Gerda and Chuang, Jody C and Liang, Gangning
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 2009, Volume 379, Issue 3, pp. 726 - 731
Studies have shown that aberrant expression of miRNAs is involved in the initiation and progression of cancer, and several miRNAs have been characterized as... 
DNA methylation | Epigenetic therapy | MicroRNA | Tumor suppressor | Cancer | METHYLATION | ACTIVATION | BIOPHYSICS | BIOCHEMISTRY & MOLECULAR BIOLOGY | Promoter Regions, Genetic | Up-Regulation | Phenylbutyrates - therapeutic use | Humans | Azacitidine - analogs & derivatives | Male | Antineoplastic Agents - therapeutic use | Azacitidine - pharmacology | Prostatic Neoplasms - genetics | Urinary Bladder Neoplasms - genetics | Neoplasms - genetics | Endothelial Growth Factors - genetics | Cell Line, Tumor | Phenylbutyrates - pharmacology | Antineoplastic Agents - pharmacology | Epigenesis, Genetic - drug effects | MicroRNAs - genetics | Gene Expression Regulation, Neoplastic - drug effects | Genes, Tumor Suppressor | Azacitidine - therapeutic use | Care and treatment | Oncology, Experimental | Cancer cells | Genetic research | Development and progression | Genetic aspects | Research | Methylation | Prostate cancer | Index Medicus
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7. Full Text Resistance to selective BRAF inhibition can be mediated by modest upstream pathway activation
by Su, Fei and Bradley, William D and Wang, Qiongqing and Yang, Hong and Xu, Lizhong and Higgins, Brian and Kolinsky, Kenneth and Packman, Kathryn and Kim, Min Jung and Trunzer, Kerstin and Lee, Richard J and Schostack, Kathleen and Carter, Jade and Albert, Thomas and Germer, Soren and Rosinski, Jim and Martin, Mitchell and Simcox, Mary Ellen and Lestini, Brian and Heimbrook, David and Bollag, Gideon
Cancer Research, ISSN 0008-5472, 02/2012, Volume 72, Issue 4, pp. 969 - 978
A high percentage of patients with BRAF(V600E) mutant melanomas respond to the selective RAF inhibitor vemurafenib (RG7204, PLX4032) but resistance eventually... 
LUNG-CANCER | ABL EXPRESSION LEVELS | MEK | AMPLIFICATION | PLX4032 | ONCOLOGY | RAS MUTATIONS | ACQUIRED-RESISTANCE | PROLIFERATION | MELANOMA-CELLS | KINASE INHIBITOR | Phosphorylation | Proto-Oncogene Proteins p21(ras) | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | Transfection | Phenylbutyrates - administration & dosage | Female | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins - metabolism | Imidazolidines - administration & dosage | Mice, SCID | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Sulfonamides - therapeutic use | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Mice | Mutation | Index Medicus
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8. Full Text Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes
by Umut Özcan and Erkan Yilmaz and Lale Özcan and Masato Furuhashi and Eric Vaillancourt and Ross O. Smith and Cem Z. Görgün and Gökhan S. Hotamisligil
Science, ISSN 0036-8075, 8/2006, Volume 313, Issue 5790, pp. 1137 - 1140
Endoplasmic reticulum (ER) stress is a key link between obesity, insulin resistance, and type 2 diabetes. Here, we provide evidence that this mechanistic link... 
Adipose tissues | Research fellowships | Obesity | Phosphorylation | Receptors | Liver | Insulin resistance | Vehicle performance | Reports | Type 2 diabetes mellitus | Insulin | ENDOPLASMIC-RETICULUM STRESS | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | DEFICIENCY | PRIMARY BILIARY-CIRRHOSIS | Phenylbutyrates - therapeutic use | eIF-2 Kinase - metabolism | Endoplasmic Reticulum - metabolism | Homeostasis | JNK Mitogen-Activated Protein Kinases - metabolism | Diabetes Mellitus, Type 2 - metabolism | Insulin - blood | Glucose - administration & dosage | Taurochenodeoxycholic Acid - pharmacology | Adipose Tissue - metabolism | Endoplasmic Reticulum - drug effects | Eukaryotic Initiation Factor-2 - metabolism | Phenylbutyrates - pharmacology | Taurochenodeoxycholic Acid - therapeutic use | Disease Models, Animal | Insulin - pharmacology | Glucose Tolerance Test | Signal Transduction | Liver - metabolism | Insulin Resistance | Animals | Cell Line, Tumor | Glucose - metabolism | Mice, Obese | Receptor, Insulin - metabolism | Mice | Enzyme Activation | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Endoplasmic reticulum | Analysis | Research | Rodents | Medical treatment | Genetics | Biochemistry | Diabetes | Index Medicus
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9. Full Text Therapeutic targeting of transcription in acute promyelocytic leukemia by use of an inhibitor of histone deacetylase
by Warrell Jr, Raymond P and He, Li-Zhen and Richon, Victoria and Calleja, Elizabeth and Pandolfi, Pier Paolo
Journal of the National Cancer Institute, ISSN 0027-8874, 11/1998, Volume 90, Issue 21, pp. 1621 - 1625
Background: Acetylation of DNA-associated histones is linked to activation of gene transcription, whereas histone deacetylation is associated with... 
CBP | TRANSLOCATION | ONCOPROTEIN | ONCOLOGY | ACETYLATION | INTERACTS | N-COR | CO-REPRESSOR | TRANS RETINOIC ACID | ACUTE MYELOID-LEUKEMIA | ACETYLTRANSFERASE | Transcription, Genetic - drug effects | Tretinoin - administration & dosage | Drug Administration Schedule | Humans | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Acetylation - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Leukemia, Promyelocytic, Acute - enzymology | Phenylbutyrates - administration & dosage | Adolescent | Fluorescent Antibody Technique | Female | Histone Deacetylases - drug effects | Leukemia, Promyelocytic, Acute - drug therapy | Acute leukemia, Promyelocytic | Care and treatment | Regulation | Genetic transcription | Enzymes | Drug therapy | Molecular biology | Leukemia | Index Medicus
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10. Full Text The levels of mutant K-RAS and mutant N-RAS are rapidly reduced in a Beclin1 / ATG5 -dependent fashion by the irreversible ERBB1/2/4 inhibitor neratinib
by Booth, Laurence and Roberts, Jane L and Poklepovic, Andrew and Kirkwood, John and Sander, Cindy and Avogadri-Connors, Francesca and Cutler Jr, Richard E and Lalani, Alshad S and Dent, Paul
Cancer Biology & Therapy, ISSN 1538-4047, 02/2018, Volume 19, Issue 2, pp. 132 - 137
The FDA approved irreversible inhibitor of ERBB1/2/4, neratinib, was recently shown to rapidly down-regulate the expression of ERBB1/2/4 as well as the levels... 
neratinib | receptor tyrosine kinase | autophagy | RAS | HDAC | ONCOLOGY | CANCER | ERBB RECEPTORS | Phenylbutyrates - therapeutic use | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Valproic Acid - pharmacology | Quinolines - pharmacology | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Neoplasms - genetics | Phenylbutyrates - pharmacology | Valproic Acid - therapeutic use | Membrane Proteins - metabolism | Receptor, ErbB-2 - antagonists & inhibitors | Drug Evaluation, Preclinical | Proto-Oncogene Proteins p21(ras) - metabolism | ErbB Receptors - antagonists & inhibitors | Membrane Proteins - genetics | Down-Regulation - drug effects | Neoplasms - drug therapy | Drug Synergism | GTP Phosphohydrolases - metabolism | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | GTP Phosphohydrolases - genetics | Autophagy-Related Protein 5 - metabolism | Cell Line, Tumor | Histone Deacetylase Inhibitors - pharmacology | Histone Deacetylase Inhibitors - therapeutic use | Quinolines - therapeutic use | Receptor, ErbB-4 - antagonists & inhibitors | Beclin-1 - metabolism | Neoplasms - pathology | Index Medicus
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11. Full Text A therapeutic strategy uses histone deacetylase inhibitors to modulate the expression of genes involved in the pathogenesis of rheumatoid arthritis
by Chung, Yih-Lin and Lee, Ming-Yuan and Wang, Ae-June and Yao, Lin-Fen
Molecular Therapy, ISSN 1525-0016, 11/2003, Volume 8, Issue 5, pp. 707 - 717
Rheumatoid arthritis (RA) is characterized by progressive destruction of the affected joints. The pathophysiology results from genetic susceptibility and... 
Histone deacetylase inhibitor | TNF-α | Cell cycle inhibitor | Rheumatoid arthritis | Gene regulation | TNF-α gene regulation | MEDICINE, RESEARCH & EXPERIMENTAL | cell cycle inhibitor | TNF-alpha | PROLIFERATION | rheumatoid arthritis | TRICHOSTATIN-A | FIBROBLASTS | FACTOR-ALPHA | TUMOR-NECROSIS-FACTOR | INTERFERON-GAMMA | gene regulation | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | histone deacetylase inhibitor | GENETICS & HEREDITY | MICE | DIFFERENTIATION | T-CELLS | SODIUM PHENYLBUTYRATE
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12. Full Text Phenylbutyrate counteracts Shigella mediated downregulation of cathelicidin in rabbit lung and intestinal epithelia: A potential therapeutic strategy
by Sarker, Protim and Ahmed, Sultan and Tiash, Snigdha and Rekha, Rokeya Sultana and Stromberg, Roger and Andersson, Jan and Bergman, Peter and Gudmundsson, Gudmundur H and Agerberth, Birgitta and Raqib, Rubhana
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 6, pp. e20637 - e20637
Background: Cathelicidins and defensins are endogenous antimicrobial peptides (AMPs) that are downregulated in the mucosal epithelia of the large intestine in... 
CELLS | CHAIN FATTY-ACIDS | IMMUNE-RESPONSES | SODIUM-BUTYRATE | BIOLOGY | ANTIMICROBIAL PEPTIDE LL-37 | GENE-EXPRESSION | RECEPTORS | PROTEIN-SYNTHESIS | TRIBUTYRIN | Lung - microbiology | Intestinal Mucosa - metabolism | Phenylbutyrates - therapeutic use | Phenylbutyrates - adverse effects | Molecular Sequence Data | Trachea - drug effects | Trachea - metabolism | Antimicrobial Cationic Peptides - metabolism | RNA, Messenger - metabolism | Shigella - drug effects | Intestinal Mucosa - drug effects | Bacterial Load - drug effects | Feces - microbiology | Intestine, Large - metabolism | Intestine, Large - microbiology | Phenylbutyrates - pharmacology | Lung - metabolism | Antimicrobial Cationic Peptides - genetics | Shigella - pathogenicity | Amino Acid Sequence | Intestine, Large - drug effects | Rabbits | Administration, Oral | Antimicrobial Cationic Peptides - chemistry | RNA, Messenger - genetics | Antimicrobial Cationic Peptides - secretion | Intestinal Mucosa - microbiology | Down-Regulation - drug effects | Dysentery, Bacillary - drug therapy | Animals | Lung - drug effects | Trachea - microbiology | Infection | Immunohistochemistry | Care and treatment | Peptides | Analysis | Communicable diseases | Esters | Health aspects | Water-borne diseases | Salmonella | Anorexia | Intravenous administration | Cathelicidins | Mucosa | Lung | Medical services | Innate immunity | Biology | Infections | Biochemistry | Immunity | Proteins | Respiratory tract | Microbiota | Metabolites | Rodents | Antimicrobial peptides | Dysentery | Colon | Trachea | Automation | Cytokines | Complications | Biophysics | Epithelium | Fatty acids | Shigellosis | Chromatography | Medicine | Sodium butyrate | Hospitals | Infectious diseases | Antibiotics | Defensins | Sodium | Protein synthesis | Large intestine | Rectum | Scientific imaging | Mass spectrometry | Phenylbutyric acid | Metabolic disorders | Index Medicus
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13. Full Text Activation of the stress proteome as a mechanism for small molecule therapeutics
by Brose, Rebecca Deering and Shin, Gloria and Mcguinness, Martina C and Schneidereith, Tonya and Purvis, Shirley and Dong, Gao X and Keefer, Jeffrey and Spencer, Forrest and Smith, Kirby D
Human Molecular Genetics, ISSN 0964-6906, 10/2012, Volume 21, Issue 19, pp. 4237 - 4252
Various small molecule pharmacologic agents with different known functions produce similar outcomes in diverse Mendelian and complex disorders, suggesting that... 
SPINAL MUSCULAR-ATROPHY | PEROXISOME PROLIFERATION | CELLULAR-RESPONSES | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | PHARMACOLOGICAL INDUCTION | FETAL-HEMOGLOBIN INDUCTION | INCREASES SMN EXPRESSION | X-LINKED ADRENOLEUKODYSTROPHY | HISTONE DEACETYLASE INHIBITORS | TRANSGENIC MOUSE MODEL | HUNTINGTONS-DISEASE | Cell Line | Thiocyanates - therapeutic use | Phenylbutyrates - therapeutic use | Proteome - genetics | Adrenoleukodystrophy - physiopathology | Humans | Drug Therapy | Small Molecule Libraries - therapeutic use | Adrenoleukodystrophy - metabolism | Mitochondrial Turnover - drug effects | Adrenoleukodystrophy - drug therapy | Hydroxamic Acids - therapeutic use | Hydroxyurea - therapeutic use | Adrenoleukodystrophy - genetics | Isothiocyanates | Proteome - metabolism | Index Medicus
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14. Full Text Ammonia control and neurocognitive outcome among urea cycle disorder patients treated with glycerol phenylbutyrate
by Diaz, George A and Krivitzky, Lauren S and Mokhtarani, Masoud and Rhead, William and Bartley, James and Feigenbaum, Annette and Longo, Nicola and Berquist, William and Berry, Susan A and Gallagher, Renata and Lichter‐Konecki, Uta and Bartholomew, Dennis and Harding, Cary O and Cederbaum, Stephen and McCandless, Shawn E and Smith, Wendy and Vockley, Gerald and Bart, Stephen A and Korson, Mark S and Kronn, David and Zori, Roberto and Merritt, J. Lawrence and C.S. Nagamani, Sandesh and Mauney, Joseph and LeMons, Cynthia and Dickinson, Klara and Moors, Tristen L and Coakley, Dion F and Scharschmidt, Bruce F and Lee, Brendan
Hepatology, ISSN 0270-9139, 06/2013, Volume 57, Issue 6, pp. 2171 - 2179
Glycerol phenylbutyrate is under development for treatment of urea cycle disorders (UCDs), rare inherited metabolic disorders manifested by hyperammonemia and... 
GASTROENTEROLOGY & HEPATOLOGY | SAFETY | DEFICIENCY | CLINICAL-TRIALS | SODIUM PHENYLBUTYRATE | CHILDREN | Glycerol - therapeutic use | Phenylbutyrates - therapeutic use | Double-Blind Method | Humans | Middle Aged | Ammonia - blood | Male | Urea Cycle Disorders, Inborn - drug therapy | Cross-Over Studies | Neuropsychological Tests | Young Adult | Glutamine - blood | Adolescent | Adult | Female | Glycerol - analogs & derivatives | Urea Cycle Disorders, Inborn - blood | Child | Index Medicus | hyperammonemia | sodium phenylbutyrate | glutamine | neuropsychological function | executive function
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