Publications

Atallah et al. Evaluation of the Correlation between Response and Duration of Treatment in a Phase 2 Study of Pracinostat Plus Azacitidine in Elderly Patients with Acute Myeloid Leukemia (AML). ASH Annual Meeting, December 2017

Takahashi et al. Treatment of Pracinostat and Azacitidine in Elderly Patients With Acute Myeloid Leukemia (AML): Correlation Between Mutation Clearance and Clinical Response. EHA Annual Congress, June 2017

Garcia-Manero et al. A Phase 2 Study of Pracinostat and Azacitidine in Elderly Patients with Acute Myeloid Leukemia (AML) Not Eligible for Induction Chemotherapy: Response and Long-Term Survival Benefit. ASH Annual Meeting, December 2016

Garcia-Manero et al. Final Results from a Phase 2 Study of Pracinostat in Combination with Azacitidine in Elderly Patients with Acute Myeloid Leukemia (AML). ASH Annual Meeting, December 2015

Garcia-Manero et al. A Randomized, Placebo-Controlled, Phase II Study of Pracinostat in Combination with Azacitidine (AZA) in Patients with Previously Untreated Myelodysplastic Syndrome (MDS). ASH Annual Meeting, December 2015

Garcia-Manero et al.Updated Results from a Phase 2 Study of Pracinostat in Combination With Azacitidine in Elderly Patients With Acute Myeloid Leukemia. EHA Annual Congress, June 2015

Garcia-Manero et al. Pracinostat in Combination with Azacitidine Produces a High Rate and Rapid Onset of Disease Remission in Patients With Previously Untreated Acute Myeloid Leukemia. ASH Annual Meeting, Dec 2014

Sooraj et al. Activated Transcription Factor 3 (ATF-3) Expression is a Potential Marker of Tumor Response to the HDAC Inhibitor Pracinostat.AACR Annual Meeting, Apr 2014

Quintas Cardama et al. Very high rates of clinical and cytogenetic response with the combination of the histone deacetylase inhibitor Pracinostat (SB939) and 5-Azacitidine in high-risk myelodysplastic syndrome.ASH Annual Meeting, Dec 2012

Quintas Cardama et al. Therapy with the histone deacetylase inhibitor Pracinostat (SB939) in patients with myelofibrosis.ASH Annual Meeting, Dec 2011

Garcia-Manero et al. Phase 1 study of the oral deacetylase inhibitor, SB939, in patients with advanced hematologic malignancies. ASH Annual Meeting, Dec 2010

Novotny-Diermayr et al. The histone deacetylase inhibitor SB939 acts synergistically with Sorafenib in an orthotopic model of hepatocellular carcinoma. AACR Annual Meeting, Apr 2010

Yong et al. Phase I study of SB939 three times weekly for 3 weeks every 4 weeks in patients with advanced solid malignancies. ASCO Annual Meeting, May 2009

Yong et al. A phase I dose escalation study of oral SB939 when administered thrice weekly (every other day) for 3 weeks in a 4-week cycle in patients with advanced solid malignancies. EORTC-NCI-AACR International Conference: Molecular Targets and Cancer Therapeutics, Oct 2008

Sangthongpitag et al. SB939: a potent and orally active HDAC inhibitor for the treatment of hematolgical malignancies.ASH Annual Meeting, Dec 2007

Sangthongpitag et al. SB939: a potent, orally active HDAC inhibitor for the treatment of haematolgic malignancies and solid tumors. AACR Centennial Conference on Translational Cancer Medicine, Nov 2007

Sangthongpitag et al. SB939: a potent and orally active HDAC inhibitor for the treatment of colorectal cancer. AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics, Oct 2007

Initial Results of a Dose Escalation Study of ME-401, a Selective and Structurally Differentiated PI3Kδ Inhibitor in Relapsed/Refractory (R/R) Follicular Lymphoma (FL) and Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma (SLL), ASCO Annual Meeting, June 2018

ME-401: A Highly Differentiated PI3Kδ-Selective Inhibitor

Zann et al. Formulation selection and development for ME-401, an oral, potent and selective inhibitor of phosphoinositide 3-kinase P110δ during a first-in-human study in healthy volunteers. AAPS Annual Meeting, Nov 2016

Moreno et al. Clinical Pharmacokinetics and Pharmacodynamics of ME-401, an Oral, Potent and Selective Inhibitor of Phosphatidylinositol 3-Kinase P110δ, Following Single Ascending Dose Administration to Healthy Volunteers. AACR Annual Meeting, Apr 2016

O'Farrell et al. Preclinical characterization of PWT143, a novel selective and potent phosphatidylinositol 3-kinase delta (PI3K delta) inhibitor with ex-vivoactivity in hematologic malignancies. ASH Annual Meeting, Dec 2012

Matthews et al. Discovery of PI3K delta inhibitors for the treatment of inflammatory and autoimmune disease. The New York Academy of Sciences: Inositol Phospholipid Signaling in Physiology and Disease, June 2012

Dey et al. Voruciclib, a clinical stage CDK inhibitor sensitizes triple negative breast cancer xenografts to proteasome inhibition. AACR Annual Meeting, April 2016

Diab et al. Phase I trial of the CDK 4/6 inhibitor, P1446A-05 (voruciclib) in combination with the BRAF inhibitor (BRAFi), vemurafenib in advanced, BRAF-mutant melanoma. ASCO Annual Meeting, June 2015

Hao et al. A phase I and pharmacokinetic (PK) study of continuous daily administration of P1446A-05, a potent and specific oral Cdk4 inhibitor. ASCO Annual Meeting, June 2012

Abrogation of resistance against bevacizumab (Bev) by mitochondrial inhibition: a phase 0 randomized trial of Bev plus ME344 or placebo in early HER2-negative breast cancer (HERNEBC), ASCO Annual Meeting, June 2018

Manevich et al. ME-344, a Novel Isoflavone with Activity as a Mitochondrial Oxygenase Inhibitor. AACR Annual Meeting, Apr 2015

Bendell et al. ME-344, a Novel Mitochondrial Oxygenase Inhibitor: Results From a First-In-Human Phase I Study.AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Oct 2013

Alvero et al. ME-344 delays tumor kinetics in an ovarian cancer in vivo recurrence model. AACR Annual Meeting, Apr 2013

Alvero et al. Depression of mitochondrial bioenergetics is a potent death stimulus in the ovarian cancer stem cells.AACR Annual Meeting, Apr 2011

Alvero et al. Targeting the mitochondria activates two independent pathways leading to caspase-independent cell death in ovarian cancer stem cells.World Congress on Targeting Mitochondria, Nov 2010

Mor et al. NV-128, a novel isoflavone derivative, targets the mTOR pathway and induces cell death in epithelial ovarian cancer stem cells. AACR Annual Meeting, Apr 2009

Mor et al. Activation of caspase-independent programmed cell death overcomes apoptosis resistance in ovarian cancer cells. AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics, Oct 2007

Alvero et al. Autophage precedes caspase-independent cell death in chemo-resistant ovarian cancer cells. AACR Annual Meeting, Apr 2007

Garcia-Manero et al. Phase 2, randomized, double-blind study of pracinostat in combination with azacitidine in patients with untreated, higher risk myelodysplastic syndromes. Cancer. 2017 Jan 17. doi: 10.1002/cncr.30533. [Epub ahead of print]

Sooraj et al. Activating Transcription Factor 3 Expression as a Marker of Response to the Histone Deacetylase Inhibitor Pracinostat. Mol Cancer Ther. 2016 Jul;15(7):1726-39.

Montalban-Bravo et al. Novel drugs for older patients with acute myeloid leukemia. Leukemia. 2015 Apr;29(4):760-9.

Bose et al. Orphan drug designation for pracinostat, volasertib and alvocidib in AML. Leuk Res. 2014 Aug;38(8):862-5.

Odenike. Beyond JAK inhibitor therapy in myelofibrosis. Hematology Am Soc Hematol Educ Program. 2013;2013:545-52.

Zorzi et al. A phase I study of histone deacetylase inhibitor, pracinostat (SB939), in pediatric patients with refractory solid tumors: IND203 a trial of the NCIC IND program/C17 pediatric phase I consortium.Pediatr Blood Cancer. 2013 Nov;60(11):1868-74.

Okabe et al. Activity of histone deacetylase inhibitors and an Aurora kinase inhibitor in BCR-ABL-expressing leukemia cells: Combination of HDAC and Aurora inhibitors in BCR-ABL-expressing cells. Cancer Cell Int. 2013 Apr 4;13(1):32.

Quintas-Cardama et al. Therapy with the histone deacetylase inhibitor pracinostat for patients with myelofibrosis. Leuk Res. 2012 Sep;36(9):1124-7.

Sumanadasa et al. Antimalarial activity of the anticancer histone deacetylase inhibitor SB939. Antimicrob Agents Chemother. 2012 Jul;56(7):3849-56.

Novotny-Diermayr et al. The oral HDAC inhibitor pracinostat (SB939) is efficacious and synergistic with the JAK2 inhibitor pacritinib (SB1518) in preclinical models of AML.Blood Cancer J. 2012 May;2(5):e69.

Jayaraman et al. Preclinical metabolism and disposition of SB939 (Pracinostat, an orally active histone deacetylase inhibitor, and prediction of human pharmacokinetics.Drug Metab Dispos. 2011 Dec;39(12):2219-32.

Yong et al. Phase I and pharmacodynamic study of an orally administered novel inhibitor of histone deacetylases, SB939, in patients with refractory solid malignancies. Ann Oncol. 2011 Nov;22(11):2516-22.

Wang et al. Discovery of (2E)-3-{2-butyl-1-[2-(diethylamino)ethyl]-1H-benzimidazol-5-yl}-N-hydroxyacrylamide (SB939), an orally active histone deacetylase inhibitor with a superior preclinical profile. J Med Chem. 2011 Jul 14;54(13):4694-720.

Novotny-Diermayr et al. Pharmacodynamic evaluation of the target efficacy of SB939, an oral HDAC inhibitor with selectivity for tumor tissue.Mol Cancer Ther. 2011 Jul;10(7):1207-17.

Razak et al. Phase I clinical, pharmacokinetic and pharmacodynamic study of SB939, an oral histone deacetylase (HDAC) inhibitor, in patients with advanced solid tumours. Br J Cancer. 2011 Mar 1;104(5):756-62.

Novotny-Diermayr et al. SB939, a novel potent and orally active histone deacetylase inhibitor with high tumor exposure and efficacy in mouse models of colorectal cancer. Mol Cancer Ther. 2010 Mar;9(3):642-52.

Paiva et al. Cyclin-Dependent Kinase Inhibitor P1446A Induces Apoptosis in a JNK/p38 MAPK-Dependent Manner in Chronic Lymphocytic Leukemia B-Cells. 2015 Nov 25;10(11):e0143685.

Manevich et al. Redox Signaling and Bioenergetics Influence Lung Cancer Cell Line Sensitivity to the Isoflavone ME-344. J Pharmacol Exp Ther. 2016 Aug;358(2):199-208.

Jeyaraju et al. A novel isoflavone, ME-344, targets the cytoskeleton in acute myeloid leukemia. Oncotarget. 2016 Jul 6. [Epub ahead of print]

Navarro et al. Targeting Tumor Mitochondrial Metabolism Overcomes Resistance to Antiangiogenics. Cell Rep. 2016 Jun 21;15(12):2705-18.

Bendell et al. Phase 1, open-label, dose escalation, safety, and pharmacokinetic study of ME-344 as a single agent in patients with refractory solid tumors. Cancer. 2015 Apr 1;121(7);1056-63.

Lim et al. Anti-cancer analogues ME-143 and ME-344 exert toxicity by directly inhibting mitochondrial NADH: ubiquinone oxidoreductase (Complex I). Am J Cancer Res. 2015;5(2):689-701.

Alvero et al. Targeting the mitochondria activates two independent cell death pathways in the ovarian cancer stem cells. Mol Cancer Ther. 2011 Aug;10(8):1385-93.

Alvero et al. NV-128, a novel isoflavone derivative, induces caspase-independent cell death through the Akt/mammalian target of rapamycin pathway.Cancer. 2009 Jul;115(14):3204-16.