IACS-010759 News - LARVOL Sigma

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|||||||||| IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] Overcoming NOTCH1-Driven Chemoresistance in T-Cell Acute Lymphoblastic Leukemia Via Metabolic Intervention with Oxphos Inhibitor (Channel 8 (Virtual Meeting)) - Nov 5, 2020 - Abstract #ASH2020ASH_4317;
In summary, we demonstrated that targeting OxPhos with IACS-010759 in combination with chemotherapy facilitates eradication of chemoresistant NOTCH1-driven T-ALL through direct targeting of the key metabolic regulators of OxPhos conferred by mutant NOTCH1 in T-ALL. Clinical trials rewiring metabolism by incorporation of OxPhos-i to standard-of-care therapy in patients with NOTCH1-mutated T-ALL are warranted to improve patients’ outcomes.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] Dual Targeting of Mitochondrial Vulnerability Using Complex I Inhibitor Iacs-010759 with Bcl-2 Inhibitor Venetoclax and Azacitidine in Pre-Clinical Acute Myeloid Leukemia (AML) Models (Poster Hall (Virtual Meeting)) - Nov 5, 2020 - Abstract #ASH2020ASH_3658;
VEN disrupts the BCL-2/VDAC interactions and reduces mitochondrial respiration, which is facilitated by the combined therapy with mitochondrial complex I inhibitor. Our preliminary findings indicate potent anti-AML activity of the dual and triple (with hypomethylating agent) combinations in vitro and in vivo.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center, Vanflyta (quizartinib) / Daiichi Sankyo
[VIRTUAL] The Combined Treatment with the FLT3-Inhibitor AC220 and the Complex I Inhibitor Iacs-010759 Synergistically Depletes Wt- and FLT3-Mutated Acute Myeloid Leukemia Cells (Poster Hall (Virtual Meeting)) - Nov 5, 2020 - Abstract #ASH2020ASH_2919;
Thus, we investigated more in-depth the synergism between IACS-010759 (10nM) and 13 FLT3 inhibitors, all currently in clinical trials (AC220, sorafenib, gilteritinib, sunitinib, ponatinib, midostaurin, ibrutinib, TP-0903, crenolanib, tandutinib, FF-10101, lestaurtinib, and KW-2449; 0.0128:5x:5000nM), in AML cell lines (FLT3-wt KG-1, U937, OCI-AML2, OCI-AML3; and FLT3-mutant MOLM-13 and MOLM-14)...Influx inhibition of both the two main carbon sources, glucose and glutamine, was observed leading to impairment of the TCA cycle and glycolysis for energy production, as well as pentose phosphate pathway and de novo nucleotide biosynthesis. In conclusion, we identified a novel drug combination AC220 and IACS-010759 which synergistically inhibits AML cell growth regardless of FLT3 mutation at least by metabolism disruption.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] The Direct Interactions with Bone Marrow Microenvironment Confer Resistance to the Inhibition of Oxidative Phosphorylation in AML (Poster Hall (Virtual Meeting)) - Nov 5, 2020 - Abstract #ASH2020ASH_1938;
We investigated how the BM microenvironment impacts the response to energy-depriving OxPhos inhibition in AML using a novel complex I OxPhos inhibitor (OxPhosi), IACS-010759...Taken together, our data highlight the importance of direct interaction with BM stromal cells as well as complementally modification of amino acid- and lipid metabolism for the resistance of AML cells to OxPhos inhibition. While the mechanisms of stroma-leukemia interactions are likely complex, reducing the adhesion of AML cells to nurturing stromal cells ameliorates the resistance to the metabolic and energetic consequences of OxPhos inhibition.

|||||||||| Avastin (bevacizumab) / Roche
[VIRTUAL] Angiogenesis inhibitors strongly synergize with therapeutics targeting tumor metabolism () - Oct 24, 2020 - Abstract #SNO2020SNO_439;
The same results were recapitulated with the anti-VEGFA antibody, Avastin, and the OxPhos inhibitor could be substituted with the Enolase inhibitor HEX, with similar effects...Together, these results suggest that Angiogenesis inhibitors synergize broadly with cancer therapies targeting metabolism, allowing the realization of the full potential of these previously disappointing drugs. Our results warrant systematic combination clinical trials between angiogenesis inhibitors and established, as well as emerging anti-metabolic cancer therapies.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] Targeting Cancer Metabolism to Enhance Tumor Radiation Response (Science Center, Oral Scientific Sessions) - Sep 13, 2020 - Abstract #ASTRO2020ASTRO_1419;
Materials/ clonogenic assay, immunoblotting, tumor regrowth delay, Seahorse studies, LC/MS Mass spectrometry We characterized novel and specific inhibitors targeting LDH enzyme A and B isoform (LDHi) and novel OXPHOS inhibitor (IACS-010759) targeting mitochondrial complex I in combination with ionizing radiation (IR) for their anti-cancer and radio-sensitization effects across various tumor types... In summary, our results presently indicate that targeting mitochondrial metabolism may be a more effective means of enhancing tumor radiosensitivity.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] Combination Treatment with Radiotherapy and a Novel Oxidative Phosphorylation Inhibitor Overcomes PD-1 Resistance and Enhances Antitumor Immunity (Poster Hall) - Sep 13, 2020 - Abstract #ASTRO2020ASTRO_1247;
In summary, our results presently indicate that targeting mitochondrial metabolism may be a more effective means of enhancing tumor radiosensitivity. OXPHOS inhibition as part of a combinatorial regimen with XRT is a promising strategy to address PD-1–resistant NSCLC, and this combination is being tested clinically.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal: A novel mitochondrial inhibitor blocks MAPK pathway and overcomes MAPK inhibitor-resistance in melanoma. (Pubmed Central) - Sep 9, 2020
OXPHOS inhibition as part of a combinatorial regimen with XRT is a promising strategy to address PD-1–resistant NSCLC, and this combination is being tested clinically. Targeting OxPhos with OPi has significant anti-tumor activity in MAPKi-resistant, BRAF-mutant melanomas, and merits further clinical investigation as a potential new strategy to overcome intrinsic and acquired resistance to MAPKi in patients.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, IACS-010759 / UT MD Anderson Cancer Center
Journal: Cotargeting of Mitochondrial Complex I and Bcl-2 Shows Antileukemic Activity against Acute Myeloid Leukemia Cells Reliant on Oxidative Phosphorylation. (Pubmed Central) - Aug 28, 2020
Consistent with our hypothesis, IACS-010759 treatment indeed retained cytochrome c in mitochondria, which was completely abolished by venetoclax, resulting in Bak/Bax- and caspase-dependent apoptosis. Our preclinical data provide a rationale for further development of the combination of IACS-010759 and venetoclax for the treatment of patients with AML.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
PK/PD data, Preclinical, Journal: Mechanism-Specific Pharmacodynamics of a Novel Complex-I Inhibitor Quantified by Imaging Reversal of Consumptive Hypoxia with [F]FAZA PET In Vivo. (Pubmed Central) - Aug 18, 2020
In this regard, IACS-010759 is a novel high affinity inhibitor of OxPhos targeting mitochondrial complex-I that has recently completed a Phase-I clinical trial in leukemia...Pilot [F]FAZA PET scans of a patient with grade IV glioblastoma yielded highly reproducible, high-contrast images of hypoxia in vivo as validated by CA-IX and GLUT-1 IHC ex vivo. Thus, [F]FAZA PET imaging provided direct evidence for the presence of consumptive hypoxia in vivo, the capacity for targeted reversal of consumptive hypoxia through the inhibition of OxPhos, and a highly-coupled mechanism-specific PD biomarker ready for translation.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Preclinical, Journal: Inhibition of Oxidative Phosphorylation Reverses Bone Marrow Hypoxia Visualized in Imageable Syngeneic B-ALL Mouse Model. (Pubmed Central) - Jul 24, 2020
Remarkably, treatment of leukemic mice with IACS-010759, a pharmacological inhibitor of mitochondrial Complex I, substantially increased pO in the BM with advanced B-ALL, and it alleviated intracellular hypoxia reported by pimonidazole staining...Our results suggest that B-ALL expansion in BM is associated with intense oxidative phosphorylation (OxPhos) leading to the onset of metabolic BM hypoxia despite increased BM vascularization. Targeting mitochondrial respiration may be a novel approach to counteract BM hypoxia in B-ALL and, possibly, tumor hypoxia in other OxPhos-reliant malignancies.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center, ibrutinib / Generic mfg.
Journal: Metabolic reprogramming toward oxidative phosphorylation identifies a therapeutic target for mantle cell lymphoma. (Pubmed Central) - Jul 16, 2020
Inhibition of OXPHOS with a clinically applicable small molecule, IACS-010759, which targets complex I of the mitochondrial electron transport chain, results in marked growth inhibition in vitro and in vivo in ibrutinib-resistant patient-derived cancer models. This work suggests that targeting metabolic pathways to subvert therapeutic resistance is a clinically viable approach to treat highly refractory malignancies.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie
Journal, IO biomarker: Electron transport chain activity is a predictor and target for venetoclax sensitivity in multiple myeloma. (Pubmed Central) - Jul 7, 2020
Further, SQR activity correlates with venetoclax sensitivity in patient samples irrespective of t(11;14) status. Use of SQR activity in a functional-biomarker informed manner may better select for MM patients responsive to venetoclax therapy.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal, IO biomarker: Molecular Profiling Reveals Unique Immune and Metabolic Features of Melanoma Brain Metastases. (Pubmed Central) - Jun 5, 2020
IACS-010759, an OXPHOS inhibitor currently in early-phase clinical trials, improved survival of mice bearing MAPK inhibitor-resistant intracranial melanoma xenografts and inhibited MBM formation in the spontaneous MBM model...IACS-010759, an OXPHOS inhibitor currently in early-phase clinical trials, improved survival of mice bearing MAPKi-resistant intracranial melanoma xenografts and inhibited MBM formation in the spontaneous MBM model. The results provide new insights into the pathogenesis and therapeutic resistance of MBMs.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
[VIRTUAL] Small molecule inhibition of mitochondrial respiration as a tumor selective therapeutic approach (Virtual Meeting II: E-Posters) - May 16, 2020 - Abstract #AACRII2020AACR-II_2650;
In particular the clinical development of IACS-010759, which targets mitochondrial complex I component ND1, by MD Anderson provides encouraging evidence that essential processes such as mitochondrial respiration can be targeted and result in patient benefits. As a potent and selective inhibitor of mitochondrial complex I, KB-00130698 adds a new tool to the chemical armamentarium in this emerging space.

|||||||||| telaglenastat (CB-839) / Calithera, IACS-010759 / UT MD Anderson Cancer Center
Metabolic switch from glycolysis to oxidative phosphorylation (ox-phos) provides survival advantage to anti-androgen-treated prostate cancer cells and make them vulnerable to mitochondrial metabolism inhibitors IACS-010759 and CB-839 (Virtual Meeting II: E-Posters) - May 16, 2020 - Abstract #AACRII2020AACR-II_1444;
These cells are more vulnerable to treatment with mitochondrial ox-phos inhibitor IACS-010759 and a glutaminase inhibitor CB-839. High-resolution microscopic analysis of CTCs has thus far been performed in 18 patient blood samples.

|||||||||| vinorelbine tartrate / Generic mfg.
Journal: Utilizing Synergistic Potential of Mitochondria-Targeting Drugs for Leukemia Therapy. (Pubmed Central) - Apr 23, 2020
Some of these four treatments were also effective in K-562, KU812 (chronic myelogenous leukemia) and CCRF-CEM, MOLT-4 (acute lymphoblastic leukemia) cells, suggesting that these treatments may have value in treating other forms of leukemia. Finally, two of the four combinations retained high synergy and strong selectivity in primary AML cells from patient samples, supporting the potential of these treatments for patients.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal: Functional Genomics Reveals Synthetic Lethality between Phosphogluconate Dehydrogenase and Oxidative Phosphorylation. (Pubmed Central) - Feb 16, 2020
Furthermore, in the OXPHOS-proficient context, blocking OXPHOS using the small-molecule inhibitor IACS-010759 enhances sensitivity to PGD inhibition in vitro and in vivo. Together, our study reveals a dependency on PGD in OXPHOS-deficient tumors that might inform therapeutic intervention in specific patient populations.

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment closed, Enrollment change, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Feb 11, 2020
P1, N=29, Active, not recruiting,  Sponsor: M.D. Anderson Cancer Center
Together, our study reveals a dependency on PGD in OXPHOS-deficient tumors that might inform therapeutic intervention in specific patient populations. Recruiting --> Active, not recruiting | N=66 --> 29

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Combined inhibition of HMG-CoA Reductase and mitochondrial oxidative phosphorylation induces tumor regression of BRAF inhibitor-resistant Melanomas. () - Nov 21, 2019 - Abstract #SMR2019SMR_196;
Molecular analysis showed that in addition to targeted inhibition of OxPhos and mevalonate pathways individually, the combination of IACS-010759 and Atorvastatin caused potent inhibition of the pro-growth and anti-apoptotic MAPK and PI3K-AKT pathways. As Atorvastatin and other clinically approved HMGCRi have wellknown safety profiles, these could be promising combinatorial agents for improving the efficacy of OxPhos inhibitors in BRAFiresistant melanomas.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Oxphos Inhibition Induces Formation of Tunneling Nanotubes in AML Cells and Facilitates Mitochondrial Transfer from BM Stroma to AML That Contributes to Microenvironment-Mediated Drug-Resistance of AML (W308, Level 3 (Orange County Convention Center)) - Nov 7, 2019 - Abstract #ASH2019ASH_6577;
Acute myeloid leukemia (AML) cells highly depend on oxidative phosphorylation (OxPhos) to satisfy their heightened demands for energy, and the complex I OxPhos inhibitor IACS-010759 (Molina, Nat...In conclusion, the findings of this study indicate an important role of mitochondria trafficking from BM stromal cells to AML cells in a compensatory adaptation to OxPhos inhibition in BM microenvironment . We propose that blocking of mitochondrial transfer could enhance the anti-AML efficacy of OxPhos targeting agents.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, azacitidine / Generic mfg., IACS-010759 / UT MD Anderson Cancer Center
Inhibiting Mitochondria Function By Bcl-2 Inhibitor Venetoclax and Complex I Inhibitor Iacs-010759 Eliminate Leukemia Cells in Pre-Clinical AML Models (Hall B, Level 2 (Orange County Convention Center)) - Nov 7, 2019 - Abstract #ASH2019ASH_5657;
Venetoclax disrupts the BCL-2/VDAC interactions and reduces mitochondrial respiration, which is facilitated by the combined therapy with mitochondrial complex I inhibitor IACS-010759. Our preliminary findings indicate potent anti-AML activity of the dual and triple (with hypomethylating agent) combinations in vitroand in vivo.

|||||||||| telaglenastat (CB-839) / Calithera, Tamoxis (tamoxifen) / Bioprofarma, IACS-010759 / UT MD Anderson Cancer Center
Glutaminase Inhibition Overcomes Acquired Resistance to Mitochondrial Complex I in NOTCH1-Driven T-Cell Acute Lymphoblastic Leukemias (T-ALL) Via Block of Glutamine Driven Reductive Metabolism (W304ABCD, Level 3 (Orange County Convention Center)) - Nov 7, 2019 - Abstract #ASH2019ASH_5121;
In summary, our findings indicate that dual blockade of metabolic processes by inhibiting complex I of mitochondria and restricting Gln utilization results in metabolic catastrophe in Notch1-mutated T-ALL associated with energy depletion and oxidative stress, which combined severely inhibit T-ALL growth and survival . We postulate that targeting this unique metabolic vulnerability of Notch1-mutated T-ALL cells constitutes a novel therapeutic modality in this aggressive malignancy.

|||||||||| Imbruvica (ibrutinib) / AbbVie, J&J
Genetically Defined Metabolic Targets Overcome Ibrutinib Resistance in Mantle Cell Lymphoma (Tangerine 2 (WF2), Level 2 (Orange County Convention Center)) - Nov 7, 2019 - Abstract #ASH2019ASH_3164;
IACS-010759, a small molecule developed by MD Anderson Cancer Center, inhibits OXPHOS and overcomes ibrutinib resistance in vitro and in PDX models . This study may pave the way to develop a PRMT5/OXPHOS-based therapeutic strategy to overcome ibrutinib resistance in MCL.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Investigating genomic and phenotypic evolution of triple negative breast cancer chemoresistance and metastasis in patient-derived xenografts (Hall 3) - Sep 23, 2019 - Abstract #SABCS2019SABCS_229;
P=N/A
Furthermore, treatment with IACS-010759, a small molecule inhibitor of electron transport chain Complex I currently in phase I clinical development, significantly delayed the regrowth of residual tumors...Furthermore, metastases exhibited reproducible enrichment of a low-abundance primary tumor transcriptomic subpopulation. Together, these studies will elucidate transcriptomic programs associated multi-organ metastasis in TNBC and are expected to enable rational therapeutic targeting strategies.

|||||||||| Avastin (bevacizumab) / Roche
Angiogenesis inhibited tumors are under anaplerotic nutrient stress which results in dramatic sensitization to metabolic therapies () - Sep 18, 2019 - Abstract #AACRNCIEORTC2019AACR_NCI_EORTC_36;
Importantly, this therapeutic synergy is not restricted to tumors with metabolic vulnerabilities, like homozygous deletions of the gene coding for Enolase 1, but is a general phenomenon. Thus, we have found a way to finally realize the long hoped-for potential of angiogenesis inhibitors in the treatment of cancer.

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment closed, Enrollment change:  Oxidative Phosphorylation Inhibitor IACS-010759 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov) -  Aug 14, 2019
P1, N=23, Active, not recruiting,  Sponsor: M.D. Anderson Cancer Center
Thus, we have found a way to finally realize the long hoped-for potential of angiogenesis inhibitors in the treatment of cancer. Recruiting --> Active, not recruiting | N=48 --> 23

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal, IO Biomarker: Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer. (Pubmed Central) - May 13, 2019
Mechanistically, we show that SMARCA4-deficient cells have a blunted transcriptional response to energy stress creating a therapeutically exploitable synthetic lethal interaction. These findings provide the mechanistic basis for further development of OXPHOS inhibitors as therapeutics against SWI/SNF mutant tumors.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal: An inhibitor of oxidative phosphorylation exploits cancer vulnerability. (Pubmed Central) - May 13, 2019
In models of brain cancer and AML, tumor growth was potently inhibited in vivo following IACS-010759 treatment at well-tolerated doses. IACS-010759 is currently being evaluated in phase 1 clinical trials in relapsed/refractory AML and solid tumors.

|||||||||| IACS-010759 / UT MD Anderson Cancer Center, Imbruvica (ibrutinib) / AbbVie, J&J
Preclinical: Our preclinical study about utilizing a drug targeting the OXPHOS metabolic pathway, IACS-010759, to overcome ibrutinib resistance was covered by @endpts #mantlecelllymphoma @MDAndersonNews (Twitter) - May 10, 2019

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Trial completion date, Trial primary completion date, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Apr 10, 2019
P1, N=60, Recruiting,  Sponsor: M.D. Anderson Cancer Center
IACS-010759 is currently being evaluated in phase 1 clinical trials in relapsed/refractory AML and solid tumors. Trial completion date: Nov 2023 --> Feb 2024 | Trial primary completion date: Nov 2023 --> Feb 2024

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Trial completion date:  Oxidative Phosphorylation Inhibitor IACS-010759 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov) -  Nov 14, 2018
P1, N=48, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Trial completion date: Nov 2023 --> Feb 2024 | Trial primary completion date: Nov 2023 --> Feb 2024 Trial completion date: Sep 2023 --> Sep 2022

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Trial completion date, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Oct 9, 2018
P1, N=60, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Trial completion date: Sep 2023 --> Sep 2022 Trial completion date: Nov 2024 --> Nov 2023

|||||||||| IACS-010759 / UT MD Anderson Cancer Center
Journal: Biological and metabolic effects of IACS-010759, an OxPhos inhibitor, on chronic lymphocytic leukemia cells. (Pubmed Central) - Jun 5, 2018
Consistent with these data, low-glucose culture conditions sensitized CLL cells to IACS-010759. Collectively, these data suggest that CLL cells adapt to use a different metabolic pathway when OxPhos is inhibited and that targeting both OxPhos and glycolysis pathways is necessary for biological effect.

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment open, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Mar 20, 2018
P1, N=60, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Collectively, these data suggest that CLL cells adapt to use a different metabolic pathway when OxPhos is inhibited and that targeting both OxPhos and glycolysis pathways is necessary for biological effect. Active, not recruiting --> Recruiting

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment closed, Enrollment change, Trial completion date, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Mar 7, 2018
P1, N=6, Active, not recruiting,  Sponsor: M.D. Anderson Cancer Center
Active, not recruiting --> Recruiting Recruiting --> Active, not recruiting | N=66 --> 6 | Trial completion date: Nov 2023 --> Nov 2024

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Trial completion date:  Oxidative Phosphorylation Inhibitor IACS-010759 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov) -  Mar 3, 2018
P1, N=48, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Recruiting --> Active, not recruiting | N=66 --> 6 | Trial completion date: Nov 2023 --> Nov 2024 Trial completion date: Sep 2022 --> Sep 2023

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment open, Trial primary completion date, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Nov 27, 2017
P1, N=66, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Trial completion date: Sep 2022 --> Sep 2023 Not yet recruiting --> Recruiting | Trial primary completion date: Feb 2024 --> Nov 2023

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
New P1 trial, Metastases:  IACS-010759 in Advanced Cancers (clinicaltrials.gov) -  Sep 24, 2017
P1, N=66, Not yet recruiting,  Sponsor: M.D. Anderson Cancer Center

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
Enrollment open:  Oxidative Phosphorylation Inhibitor IACS-010759 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov) -  Oct 3, 2016
P1, N=48, Recruiting,  Sponsor: M.D. Anderson Cancer Center
Not yet recruiting --> Recruiting | Trial primary completion date: Feb 2024 --> Nov 2023 Not yet recruiting --> Recruiting

||||||||||  IACS-010759 / UT MD Anderson Cancer Center
New P1 trial:  Oxidative Phosphorylation Inhibitor IACS-010759 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov) -  Aug 28, 2016
P1, N=48, Not yet recruiting,  Sponsor: M.D. Anderson Cancer Center



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