This is a prospective randomized placebo-controlled double-blind crossover study determining the effect of dichloroacetate on brain glucose metabolism under clamped hypoglycemia in T1DM.

Start Date01 Jan 2024

Sponsor / Collaborator

Yale University

NCT05120284 / RecruitingPhase 2IIT

Trial of Dichloroacetate (DCA) in Glioblastoma Multiforme (GBM)

Conduct a multicenter, open label Phase IIA trial of oral DCA in 40 surgical patients with recurrent GBM who have clinically indicated debulking surgery planned. No patients will be recruited at UF. Patients will be genotyped to establish safe dosing regimens and will be randomized to receive DCA (N=20) or no DCA (N=20) for one week prior to surgery. Deidentified blood and tumor tissue obtained at surgery will be assessed at UF for biochemical markers of DCA dynamics.

Start Date01 Jul 2022

Sponsor / Collaborator

University of Florida

[+1]

NCT02616484 / Active, not recruitingPhase 3IIT

Phase 3 Trial of Dichloroacetate in Pyruvate Dehydrogenase Complex Deficiency:

The objective of this research study is to conduct a pivotal phase 3 trial of treatment with the investigational drug dichloroacetate (DCA) in young children with deficiency of the pyruvate dehydrogenase complex (PDC). PDC deficiency (PDCD) is the most common cause of congenital lactic acidosis and is a frequently fatal metabolic disease of childhood for which no proven treatment exists. The investigators predict that DCA represents targeted potential therapy for PDCD because of its ability to increase both the catalytic activity and stability of the enzyme complex. The conclusions of numerous laboratory and clinical investigations are consistent with this postulate and have led to the designation of DCA as an Orphan Product for congenital lactic acidosis by the Food and Drug Administration.
A novel Observer reported outcome (ObsRO) survey that is completed by study participant's parent/caregiver, is the efficacy outcome measure.
Funding Source - FDA OOPD

Start Date14 Jul 2020

Sponsor / Collaborator

University of Florida

[+3]

100 Clinical Results associated with Sodium Dichloroacetate

100 Translational Medicine associated with Sodium Dichloroacetate

100 Patents (Medical) associated with Sodium Dichloroacetate

3,056

Literatures (Medical) associated with Sodium Dichloroacetate

01 Mar 2024·Environmental research

Assessing the trophic ecology and migration on the exposure of cape petrels and Wilson's storm petrels from Antarctica to perfluoroalkylated substances, trace and major elements

Article

Author: Eens, M ; Leite, A ; Lepoint, G ; Das, K ; Bervoets, Lieven ; Padilha, J A G ; Souza-Kasprzyk, J ; Costa, E S ; Groffen, T ; Santos, S ; Pessôa, A R ; Cunha, L S T ; Torres, J P M ; E, Prinsen ; Dorneles, P R ; Willems, T

Chemical pollution is a global concern as contaminants are transported and reach even the remote regions of Antarctica. Seabirds serve as important sentinels of pollution due to their high trophic position and wide distribution. This study examines the influence of migration and trophic ecology on the exposure of two Antarctic seabirds, Wilson's storm petrel (Oceanites oceanicus - Ooc), and Cape petrel (Daption capense - Dca), to chemical elements and perfluoroalkyl substances (PFAS). Our methodology involved assessing the concentration of these pollutants in feather samples obtained from carcasses, offering a practical means for monitoring contamination. Trace and major element concentrations were comparable in both species, suggesting that migratory patterns have a minimal impact on exposure levels. However, Ooc had higher concentration of PFAS compared to Dca (mean, ng g^-1dry weight, PFOA: Ooc:0.710, Dca:0.170; PFTrDA: Ooc:0.550, Dca:0.360, and PFTeDA: Ooc:1.01, Dca:0.190), indicating that migration to the more polluted Northern Hemisphere significantly affects PFAS exposure. Furthermore, while no strong associations were found between either trace elements or PFAS and the three stable isotopes (δ¹³C, δ¹⁵N, and δ³⁴S), a negative association was observed between PFUnDA and δ¹⁵N, hinting at potential biodilution. The research concludes that the migratory patterns of these seabird species affect their PFAS exposure, underscoring the critical need for further exploration and understanding of these relationships to better inform conservation strategies.

01 Mar 2024·Fish & shellfish immunology

Bile acid and short chain fatty acid metabolism of gut microbiota mediate high-fat diet induced intestinal barrier damage in Macrobrachium rosenbergii

Article

Author: Sun, Cunxin ; Zheng, Xiaochuan ; Chen, Jianming ; Yang, Jie ; Liu, Bo ; Liu, Mingyang ; Yuan, Meng ; Zhou, Qunlan ; Xu, Xiaodi

The limited tolerance of crustacean tissue physiology to a high-fat diet has captured the attention of researchers. Yet, investigations into the physiological response mechanisms of the crustacean intestinal barrier system to a high-fat diet are progressing slowly. Elucidating potential physiological mechanisms and determining the precise regulatory targets would be of great physiological and nutritional significance. This study established a high-fat diet-induced intestinal barrier damage model in Macrobrachium rosenbergii, and systematically investigated the functions of gut microbiota and its functional metabolites. The study achieved this by monitoring phenotypic indicators, conducting 16S rDNA sequencing, targeted metabolomics, and in vitro anaerobic fermentation of intestinal contents. Feeding prawns with control and high-fat diets for 8 weeks, the lipid level of 7 % in the CON diet and 12 % in the HF diet. Results showed that high-fat intake impaired the intestinal epithelial cells, intestinal barrier structure, and permeability of M. rosenbergii, activated the tight junction signaling pathway inhibiting factor NF-κB transcription factor Relish/myosin light chain kinase (MLCK), and suppressed the expression of downstream tight junction proteins zona occludens protein 1 (ZO-1) and Claudin. High-fat intake resulted in a significant increase in abundance of Aeromonas, Enterobacter, and Clostridium sensu stricto 3 genera, while Lactobacillus, Lactococcus, Bacteroides, and Ruminococcaceae UCG-010 genera were significantly decreased. Targeted metabolomics results of bile acids and short-chain fatty acids in intestinal contents and in vitro anaerobic fermentation products showed a marked rise in the abundance of DCA, 12-KetoLCA, 7,12-diketoLCA, and Isovaleric acid, and a significant reduction in the abundance of HDCA, CDCA, and Acetate in the HF group. Pearson correlation analysis revealed a substantial correlation between various genera (Clostridium sensu stricto 3, Lactobacillus, Bacteroides) and secondary metabolites (DCA, HDCA, 12-KetoLCA, Acetate), and the latter was significantly correlated with intestinal barrier function related genes (Relish, ZO-1, MLCK, vitamin D receptor, and ecdysone receptor). These findings indicate that gut microorganisms and their specific bile acids and short-chain fatty acid secondary metabolites play a crucial role in the process of high-fat-induced intestinal barrier damage of M. rosenbergii. Moreover, identifying and targeting these factors could facilitate precise regulation of high-fat nutrition for crustaceans.

01 Feb 2024·Drug metabolism and disposition: the biological fate of chemicals

Comparison of 1Beta- and 5Beta-hydroxylation of Deoxycholate and Glycodeoxycholate as In Vitro Index Reactions for Cytochrome P450 3A Activities

Article

Author: Zeng, Wushuang ; Wei, Wei ; Cheng, Bin ; Wang, Yutong ; Chen, Qi ; Gui, Lanlan ; Miao, Jia ; Xu, Liang ; Lan, Ke ; Wang, Cuitong ; Wang, Yixuan

Cytochrome P450 3A (CYP3A) participates in the metabolism of more than 30% of clinical drugs. The vast intra- and inter-individual variations in CYP3A activity pose great challenges to drug development and personalized medicine. It has been disclosed that human CYP3A4 and CYP3A7 are exclusively responsible for the tertiary oxidations of deoxycholic acid (DCA) and glycodeoxycholic acid (GDCA) regioselectivity at C-1β and C-5β This work aimed to compare the 1β- and 5β-hydroxylation of DCA and GDCA as potential in vitro CYP3A index reactions in both human liver microsomes and recombinant P450 enzymes. The results demonstrated that the metabolic activity of DCA 1β- and 5β-hydroxylation was 5-10 times higher than that of GDCA, suggesting that 1β-hydroxyglycodeoxycholic acid and 5β-hydroxyglycodeoxycholic acid may originate from DCA oxidation followed by conjugation in humans. Metabolic phenotyping data revealed that DCA 1β-hydroxylation, DCA 5β-hydroxylation, and GDCA 5β-hydroxylation were predominantly catalyzed by CYP3A4 (>80%), while GDCA 1β-hydroxylation had approximately equal contributions from CYP3A4 (41%) and 3A7 (58%). Robust Pearson correlation was established for the intrinsic clearance of DCA 1β- and 5β-hydroxylation with midazolam (MDZ) 1'- and 4-hydroxylation in fourteen single donor microsomes. Although DCA 5β-hydroxylation exhibited a stronger correlation with MDZ oxidation, DCA 1β-hydroxylation exhibited higher reactivity than DCA 5β-hydroxylation. It is therefore suggested that DCA 1β- and 5β-hydroxylations may serve as alternatives to T 6β-hydroxylation as in vitro CYP3A index reactions. SIGNIFICANCE STATEMENT: The oxidation of DCA and GDCA is primarily catalyzed by CYP3A4 and CYP3A7. This work compared the 1β- and 5β-hydroxylation of DCA and GDCA as in vitro index reactions to assess CYP3A activities. It was disclosed that the metabolic activity of DCA 1β- and 5β-hydroxylation was 5-10 times higher than that of GDCA. Although DCA 1β-hydroxylation exhibited higher metabolic activity than DCA 5β-hydroxylation, DCA 5β-hydroxylation demonstrated stronger correlation with MDZ oxidation than DCA 1β-hydroxylation in individual liver microsomes.

News (Medical) associated with Sodium Dichloroacetate

03 Oct 2023

·www.sciencedaily.com

A promising treatment on the horizon for cancer-related fatigue

Cancer-related fatigue is a debilitating yet all-too-common condition, which can severely affect quality of life for patients undergoing treatment. For those struggling with CRF, there have been no effective pharmaceutical treatments for the constellation of symptoms that together define the syndrome. Researchers found that a metabolism-targeting drug called dichloroacetate (DCA) helped alleviate CRF in mice, without interfering with cancer treatments. Cancer-related fatigue (CRF) is a debilitating yet all-too-common condition, which can severely affect quality of life for patients undergoing treatment. For those struggling with CRF, there have been no effective pharmaceutical treatments for the constellation of symptoms that together define the syndrome. In a new study led by Yale Cancer Center researchers at Yale School of Medicine, the team found that a metabolism-targeting drug called dichloroacetate (DCA) helped alleviate CRF in mice, without interfering with cancer treatments. The findings are a pathway for future CRF research that may someday lead to a new therapy for patients. The results were published in American Journal of Physiology-Endocrinology and Metabolism on Oct. 2. "This study identifies dichloroacetate, an activator of glucose oxidation, as the first intervention, and particularly the first metabolism-focused intervention, to prevent the whole syndrome of cancer-related fatigue in preclinical models," said senior author Rachel Perry, who is a member of Yale Cancer Center. Researchers used tumor-bearing mouse models to investigate the effectiveness of DCA in treating cancer-related fatigue for patients living with melanoma. The group found that DCA did not affect the rates of tumor growth or compromise the effectiveness of immunotherapy or chemotherapy in two mouse cancer models. DCA also significantly preserved physical function and motivation in mice with late-stage tumors. The data suggests that DCA treatment may have several positive effects, including reducing oxidative stress in muscle tissue of tumor-bearing mice. The researchers said DCA could be a practice-changing approach in the future, when used as an adjuvant therapy to treat cancer-related fatigue. "We hope that this research will provide the bedrock for future clinical trials using dichloroacetate -- an FDA-approved drug for another indication (lactic acidosis) -- to treat the debilitating syndrome of cancer-related fatigue," said Perry, who is also an assistant professor of medicine (endocrinology) and of cellular and molecular physiology at Yale School of Medicine.

16 Mar 2023

·www.biospace.com

Saol Therapeutics enhances its IP portfolio for Dichloroacetate (DCA; SL-1009) in Glioblastoma and Rare Pediatric Cancers

By signing an agreement with Medosome Biotec By providing support for clinical trial treatment of GBM at the University of Florida By starting a collaborative research project in rare pediatric cancers with a leading cancer center ROSWELL, Ga, DUBLIN and HAMILTON, Bermuda, March 16, 2023 /PRNewswire/ -- Saol Therapeutics ("Saol"), a privately held, clinical-stage pharmaceutical company, announced today the signing of an agreement with Medosome Biotec, LLC to provide Saol the rights to use their patented genotype test for all potential indications where SL-1009 might be used as a therapy. The test is performed to identify potential mutations at GSTZ1 (glutathione S-transferase zeta 1 human enzyme) that categorize individuals as fast or slow metabolizers of DCA (SL-1009). Utilization of the genotype testing enables individual dosing, potentially reducing the incidence of treatment related adverse events. Prior to this agreement Saol only had rights to the patented genotype test for the indication of Pyruvate Dehydrogenase Complex Deficiency (PDCD). "We are pleased to have executed these agreements to support our pursuit of expanded opportunities beyond PDCD" As part of the agreement Saol will aid patient recruitment efforts for the Phase IIA Trial of DCA in Glioblastoma Multiforme (GBM) by providing additional funding and resource support. Glioblastoma is aggressive and the most common type of primary brain cancer in adults. GBM is difficult to treat and there is no known cure. This study, sponsored by the University of Florida and the Food and Drug Administration (FDA) (NCT05120284), is further supported in partnership with Medosome Biotec and Saol. Dr. Peter Stacpoole is Principal Investigator for the PDCD trial and the GBM trial and is Professor of Medicine at University of Florida. Dr. Stacpoole stated, "We are pleased to expand our partnership with Saol Therapeutics. Our partnership has led to over-enrollment of our Phase III study in PDCD (NCT02616484) and we mutually see the broader potential application of DCA as the prototypic inhibitor of Pyruvate Dehydrogenase Kinases (PDKs) that, in turn, inhibit PDC enzymatic activity. We look forward to collaborating with Saol on potential additional indications for DCA. Expansion of our collaboration on the GBM trial will result in the addition of more study sites, allowing for quicker recruitment of patients. We are hopeful that DCA will be an important addition to the treatment of GBM." Saol also recently signed a sponsored research agreement with a leading cancer center to evaluate DCA in rare pediatric solid tumors. The preclinical research will investigate DCA alone and in combination with chemotherapy in several different pediatric tumor models, such as Wilms, Neuroblastoma, Rhabdoid Tumor, Osteosarcoma, Ewing Sarcoma, and Rhabdomyosarcoma. Literature suggests that DCA could be effective in several rare, pediatric, solid tumors. The rationale for the pediatric tumor screening includes the fact that DCA has been widely studied in animals and humans and has a mechanism of action that might override the Warburg effect seen in cancer cells1,2,3,4. Saol is currently studying this medicine in children using a proprietary formulation developed for pediatric use (NCT02616484). "If the pre-clinical assessment provides encouraging data, the work already conducted in pediatric patients may allow us to quickly transition toward clinical investigation", commented Dr. Virinder Nohria, Chairman and Chief Medical Officer at Saol. These agreements, and the additional investments behind them, represent an important next step in the evolution of Saol Therapeutics as an emerging pharmaceutical company. "Now that we have completed enrollment in the PDCD trial we are rapidly transitioning to other important therapeutic areas, and are evaluating the utility of DCA (SL-1009) in adult and pediatric oncology indications with limited treatment options", said Saol CEO David Penake. "We are pleased to have executed these agreements to support our pursuit of expanded opportunities beyond PDCD". Saol expects to have topline data in the PDCD trial in the 3rd quarter of 2023. Should the results of the trial support a subsequent FDA approval, it will be the first and only medicine approved for this rare, pediatric indication. References Aminzadeh S, Vidali S, Sperl W, Kofler B, Feichtinger RG. Energy metabolism in neuroblastoma and Wilms tumor. Transl Pediatr. 2015 Jan;4(1):20-32. doi: 10.3978/j.issn.2224-4336.2015.01.04. Guo JQ, Tang HY, Wang CD, Sang BT, Liu X, Yi FP, Liu GL, Wu XM. Influence of Dichloroacetate on Wilms' Tumor in vitro. Ann Clin Lab Sci. 2022 Jan;52(1):101-108. PMID: 35181623. Kankotia S, Stacpoole PW. Dichloroacetate and cancer: new home for an orphan drug? Biochim Biophys Acta. 2014 Dec;1846(2):617-29. doi: 10.1016/j.bbcan.2014.08.005. Tataranni T, Piccoli C. Dichloroacetate (DCA) and Cancer: An Overview towards Clinical Applications. Oxid Med Cell Longev. 2019 Nov 14;2019:8201079. doi: 10.1155/2019/8201079. PMID: 31827705. About Dichloroacetate (DCA; SL-1009) DCA, a pan- PDK inhibitor, has the potential to be the 1st approved medication for the mitochondrial disease PDCD and will be available as an oral solution. Gene mutations in the mitochondrial Pyruvate Dehydrogenase Complex (PDC) lead to congenital PDCD. However, PDC is also inhibited by PDKs, that may be over-expressed in PDCD. DCA inhibits PDKs to stimulate residual PDC activity and increase energy (ATP) production by mitochondria. DCA dosing is based on a proprietary genetic test that dichotomizes subjects into "fast" and "slow" drug metabolizers, providing individualized dosing. About Saol Therapeutics Saol Therapeutics (pronounced "Sail") is a privately held, clinical-stage, pharmaceutical company with operations in Roswell, GA, Dublin, Ireland and Hamilton, Bermuda. Saol is focused on development activity in CNS disorders such as spasticity and pain management, and orphan diseases. Saol is committed to providing and advancing therapeutic options for patients and the physicians treating these populations. For more information, visit . About Medosome Biotec Medosome Biotec, LLC is a privately held, preclinical and early-stage clinical pharmaceutical company with operations in Alachua, FL and Bloomington, IN. The Company focuses on pediatric diseases with an emphasis on developing and offering genetic tests for diagnosing rare diseases and providing personalized dosing of pharmaceutical drugs. For more information, visit Media contact: Brian Nappi, Senior Vice President Strategy, bnappi@saolrx.com

Phase 2License out/inOrphan DrugDrug Approval

04 Oct 2022

·www.biospace.com

Saol Therapeutics Announces Enrollment Achievement in Pivotal Phase 3 Trial for Rare Mitochondrial Disease - Pyruvate Dehydrogenase Complex Deficiency (PDCD)

ROSWELL, Ga. and DUBLIN and HAMILTON, Bermuda, Oct. 4, 2022 /PRNewswire/ -- Saol Therapeutics, a privately held, clinical-stage pharmaceutical company, announced today that the pivotal Phase 3 clinical trial evaluating Sodium Dichloroacetate (DCA) for the treatment of a rare, pediatric, ultra-orphan mitochondrial disease, Pyruvate Dehydrogenase Complex Deficiency (PDCD) has achieved its targeted enrollment. Saol is one of the trial collaborators, with topline results anticipated early in the second half of 2023. "I began working on a treatment for PDCD in the 1980s so it is extremely rewarding to finally reach this milestone" "There are many challenges to overcome when enrolling patients in clinical trials for rare diseases", said Saol Therapeutics CEO David Penake. "The hard work of the individual study sites, patient advocacy groups, genetic testing companies, and genetic counseling partners allowed us to exceed our enrollment target of 30 patients. Our team will now prepare for a rapid NDA submission should the treatment prove to be successful." This investigator-initiated, NIH and FDA funded trial, conducted in close partnership with University of Florida, Saol Therapeutics and Medosome Biotec, represents the culmination of years of work for Dr. Peter Stacpoole, Principal Investigator and Professor of Medicine at University of Florida. "I began working on a treatment for PDCD in the 1980s after a family in Connecticut contacted me to see if I could help their child, so it is extremely rewarding to finally reach this milestone", said Stacpoole. Philip E. Yeske, Ph.D., Science & Alliance Officer at United Mitochondrial Disease Foundation, commented "The mitochondrial disease patient community is deeply appreciative of the time, effort, and capital that Saol and its collaborators are investing into this project. An over-enrolled clinical trial is a testament to the desire of the PDCD patient families to play an active role in therapeutic development." Study Design This trial evaluates daily administration of DCA in children with a confirmed pathological mutation in the Pyruvate Dehydrogenase Complex or in a pyruvate dehydrogenase phosphatase gene. The primary efficacy outcome measure is based on a novel Observer Reported Outcome (ObsRO) survey developed specifically for this trial. The study design is a 9-month double-blind crossover comparison between DCA and placebo, during which the ObsRO is completed daily by a parent/caregiver, followed by an open label phase of DCA administration. More information on the clinical trial and participating institutions can be found at Phase 3 PDCD Trial. About DCA (SL-1009) DCA has the potential to be the 1st approved medication for the mitochondrial disease PDCD and will be available as an oral solution. Gene mutations in the mitochondrial Pyruvate Dehydrogenase Complex (PDC) lead to congenital PDCD. However, PDC is also inhibited by pyruvate dehydrogenase kinases (PDK), that may be over-expressed in PDCD. DCA inhibits PDKs to stimulate residual PDC activity and increase energy (ATP) production by mitochondria. DCA dosing is based on a proprietary genetic test that dichotomizes subjects into "fast" and "slow" drug metabolizers, providing individualized dosing. About Pyruvate Dehydrogenase Complex Deficiency (PDCD) PDCD is a mitochondrial disorder of carbohydrate oxidation that mostly affects the nervous system and skeletal muscle and leads to decreased ATP production and energy failure. It affects only a few hundred individuals in the U.S. It is a common cause of congenital lactic acidosis, a life-threatening condition that may occur as early as the neonatal period. Patients may also exhibit extreme tiredness (lethargy), poor feeding, and rapid breathing (tachypnea)and other signs of neurological and neuromuscular dysfunction, such as developmental delay, low muscle tone (hypotonia), abnormal eye movements and seizures. Signs and symptoms usually begin soon after birth but may appear later in childhood. There are currently no FDA-approved therapies for PDCD. About Saol Therapeutics Saol Therapeutics (pronounced "Sail") is a privately held, clinical-stage, pharmaceutical company with operations in Roswell, GA, Dublin, Ireland and Hamilton, Bermuda. Saol is focused on development activity in CNS disorders such as spasticity and pain management, and orphan diseases. Saol is committed to providing and advancing therapeutic options for patients and the physicians treating these populations. For more information, visit . About Medosome Biotec Medosome Biotec, LLC is a privately held, preclinical and early-stage clinical pharmaceutical company with operations in Alachua, FL. The Company focuses on pediatric diseases with an emphasis on developing and offering genetic tests for diagnosing rare diseases and providing personalized dosing of pharmaceutical drugs. For more information, visit View original content: SOURCE Saol Therapeutics

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100 Deals associated with Sodium Dichloroacetate

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KEGG	Wiki	ATC	Drug Bank
D05857	Sodium Dichloroacetate	-	DB08809

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Pyruvate Dehydrogenase Complex Deficiency Disease	Phase 3	US	Medosome Biotec LLC	14 Jul 2020
Pyruvate Dehydrogenase Complex Deficiency Disease	Phase 3	US	Saol Therapeutics, Inc.	14 Jul 2020
Congenital lactic acidosis	Phase 3	-	University of Florida	01 Oct 1998
Acidosis, Lactic	Phase 3	-	The Valens Co., Inc.	-
Acidosis, Lactic	Phase 3	-	Mallinckrodt Plc	-
Brain Injuries, Traumatic	Phase 3	-	The Valens Co., Inc.	-
Brain Injuries, Traumatic	Phase 3	-	Mallinckrodt Plc	-
Myocardial Ischemia	Phase 3	-	Mallinckrodt Plc	-
Myocardial Ischemia	Phase 3	-	The Valens Co., Inc.	-
Stroke	Phase 3	-	Mallinckrodt Plc	-

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01386632 (Pubmed) Manual	Phase 2	Locally Advanced Head and Neck Squamous Cell Carcinoma	45	Chemoradiotherapy+dichloroacetate	ykswizsyxj(ysgbycqlfi) = However, there were no significant differences in grade 3/4 AE rates. ypshuogyal (izvvwykaie ) View more	Positive	21 Mar 2022
				Placebo
NCT01386632 (CTgov)	Phase 2	Advanced Head and Neck Carcinoma \| Squamous Cell Carcinoma of Head and Neck	50	DCA (dichloroacetate) (DCA (Dichloroacetate) Treatment)	asbjhuqsaa(viabyuvdwc) = fgurhmybvu uodasmgcnl (kyzzdcfytg, esqfbmsqmp - ujgfkjfnbe) View more	-	14 Jun 2017
				Placebo (Placebo)	asbjhuqsaa(viabyuvdwc) = ymlzkzkcjh uodasmgcnl (kyzzdcfytg, aonvpdvyzd - ojkhtlsjcp) View more
NCT01029925 (CTgov)	Phase 2	Metastatic breast cancer	7	Dichloroacetate (DCA)	unkhiapfmy(omyzixsajm) = lemigchini baszguzoqn (ffgvzdcsac, nsmkhpaypq - dfxkymeqcn) View more	-	12 Feb 2016
NCT01386632 (ASCO2015)	Phase 2	Locally Advanced Head and Neck Squamous Cell Carcinoma	50	Dichloroacetate (DCA)	ipqxbalmpn(qvwfvwuvxb) = not significantly different (16% DCA vs 4% P; p = 0.35) xvrsvdnytg (eysyafvmoo ) View more	-	20 May 2015
				Placebo
NCT01029925 (Pubmed \| J Cancer Res Clin Oncol)	Phase 2	Hypoxia \| Advanced Lung Non-Small Cell Carcinoma	7	Dichloroacetate	ibmqpycdjn(chyrqecega) = two patients had disease progression prior to the first scheduled scans ykkzbouyij (fcshrogztn ) View more	-	01 Mar 2014
AACR2012	Not Applicable	Breast Cancer	-	Dichloroacetate (DCA)	nrgtdkrxxt(vfkoveszba) = rorgnsnayf csjtqigxcw (gienyilybb )	-	15 Apr 2012

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