Sumitomo Dainippon Pharma Oncology (SDP Oncology) is committed to advancing translational research on novel pathways in order to develop meaningful medicines for patients with cancer.
- *Napabucasin is also known as BBI-608.
- †Active, not recruiting.
- ‡BBI-503 is also known as Amcasertib.
- §Alvocidib was formerly known as flavopiridol.
- ||DSP-7888 is also known as ombipepimut-S and adegramotide/nelatimotide.
- Additional, ongoing clinical trials conducted in Japan by Sumitomo Dainippon Pharma Co., Ltd., are not listed on this website. For information about these trials, please visit https://www.ds-pharma.com/rd/clinical/pipeline.html
- All compounds are investigational agents, and their safety and efficacy have not been established. There is no guarantee that any of these agents will receive health authority approval or become commercially available in any country for the uses being investigated
- For additional information on clinical studies, including studies that are actively recruiting, please see www.clinicaltrials.gov or contact us
- To learn more about SDP Oncology’s Expanded Access and Compassionate Use Policy, please visit our guidelines
ACM=alvocidib, cytarabine, and mitoxantrone; ACVR1=activin A receptor type 1; AML=acute myeloid leukemia; AXL=member of the Tyro3-Axl-Mer (TAM) subfamily; BCL-2=B-cell lymphoma 2; BMP=bone morphogenic protein; CDK=cyclin-dependent kinase; CTLA4=cytotoxic T-lymphocyte–associated protein 4; CTL=cytotoxic T lymphocyte; DIPG=diffuse intrinsic pontine glioma; MCL-1=myeloid cell leukemia 1; MDS=myelodysplastic syndromes; NK cells=natural killer cells; NQO1=NAD(P)H:quinone oxidoreductase 1; PD1=programmed cell death protein 1; PIM=proviral integration site for Moloney murine leukemia virus; PK=pyruvate kinase; PKM2=pyruvate kinase M2 isoform; ROS=reactive oxygen species; RTK=receptor tyrosine kinase; TLR=Toll-like receptor; TGF-β =transforming growth factor–beta; TNK=tyrosine kinase non-receptor; WT1=Wilms’ tumor 1.
- Chang AY, Hsu E, Patel J, et al. Evaluation of tumor cell-tumor microenvironment component interactions as potential predictors of patient response to napabucasin. Mol Cancer Res. 2019;17(7):1429-1434.
- Froeling F, Swamynathan MM, Deschênes A, et al. Bioactivation of napabucasin triggers reactive oxygen species-mediated cancer cell death. Clin Cancer Res. 2019;25(23):7162-7174.
- Madajewski B, Boatman MA, Chakrabarti G, Boothman DA, Bey EA. Depleting tumor-NQO1 potentiates anoikis and inhibits growth of NSCLC. Mol Cancer Res. 2016;14(1):14-25.
- Yeh YY, Chen R, Hessler J, et al. Up-regulation of CDK9 kinase activity and Mcl-1 stability contributes to the acquired resistance to cyclin-dependent kinase inhibitors in leukemia. Oncotarget. 2015;6(5):2667-2679.
- Yin T, Lallena MJ, Kreklau EL, et al. A novel CDK9 inhibitor shows potent antitumor efficacy in preclinical hematologic tumor models. Mol Cancer Ther. 2014;13(6):1442-1456.
- Boffo S, Damato A, Alfano L, Giordano A. CDK9 inhibitors in acute myeloid leukemia. J Exp Clin Cancer Res. 2018;37(1):36.
- Chen R, Keating MJ, Gandhi V, Plunkett W. Transcription inhibition by flavopiridol: mechanism of chronic lymphocytic leukemia cell death. Blood. 2005;106(7):2513-2519.
- Zeidner JF, Foster MC, Blackford AL, et al. Randomized multicenter phase II study of flavopiridol (alvocidib), cytarabine, and mitoxantrone (FLAM) versus cytarabine/daunorubicin (7+3) in newly diagnosed acute myeloid leukemia. Haematologica. 2015;100(9):1172-1179.
- Zeidner J, Lee D, Frattini M, et al. Zella-101: phase 1 study of alvocidib followed by 7+3 induction in newly diagnosed AML. Poster presented at: EHA25; June 11-21, 2020; Digital.
- Goto M, Nakamura M, Suginobe N, et al. DSP-7888, a novel cocktail design of WT1 peptide vaccine, and its combinational immunotherapy with immune checkpoint-blocking antibody against PD-1. Blood. 2016;128(22):4715.
- Miyakoshi S, Usuki K, Matsumura I, et al. Preliminary results from a phase 1/2 study of DSP-7888, a novel WT1 peptide-based vaccine, in patients with myelodysplastic syndrome (MDS). Blood. 2016:128(22):4335.
- Kijima N, Hashimoto N, Chiba Y, Fujimoto Y, Sugiyama H, Yoshimine T. Functional roles of Wilms’ tumor 1 (WT1) in malignant brain tumors. In: van den Heuvel-Eibrink M, ed. Wilms Tumor. Brisbane, Australia: Codon Publications; 2016:261-272
- Qi XW, Zhang F, Wu H, et al. Wilms' tumor 1 (WT1) expression and prognosis in solid cancer patients: a systematic review and meta-analysis. Sci Rep. 2015;5(8924).
- Chidambaram A, Fillmore HL, Van Meter TE, Dumur CI, Broaddus WC. Novel report of expression and function of CD97 in malignant gliomas: correlation with Wilms tumor 1 expression and glioma cell invasiveness. J Neurosurg. 2012;116(4):843-853.
- Oka Y, Tsuboi A, Nakata J, et al. Wilms’ tumor gene 1 (WT1) peptide vaccine therapy for hematological malignancies: from CTL epitope identification to recent progress in clinical studies including a cure-oriented strategy. Oncol Res Treat. 2017;40:682-690.
- Spira A, et al., Multicenter, open-label, phase 1 study of DSP-7888 Dosing Emulsion (DSP-7888) in patients with advanced malignancies. 2019. SITC. Abstract #355.
- Park IK, Mundy-Bosse B, Whitman SP, et al. Receptor tyrosine kinase Axl is required for resistance of leukemic cells to FLT3-targeted therapy in acute myeloid leukemia. Leukemia. 2015;29(12):2382-2389.
- Soh KK, Kim W, Lee YS, et al. Abstract 235: AXL inhibition leads to a reversal of a mesenchymal phenotype sensitizing cancer cells to targeted agents and immune-oncology therapies. Exp Mol Ther. 2016;76(14 suppl).
- Brand T, Lida M, Stein A, et al. AXL is a logical molecular target in head and neck squamos cell carcinoma. Clin Cancer Res. 2015;21(11):2601-2616.
- Rankin E, Giaccia A. The receptor tyrosine kinase AXL in cancer progression. Cancers (Basel). 2016;8(103).
- Soh KK, Bahr BL, Bearss JJ, et al. Inhibition of Axl kinase reverses the mesenchymal phenotype in leukemic cells through the disruption of retinoic signaling [Abstract]. Blood. 2015;126:3253.
- Ota Y, Otsubo T, Koroki J, et al. Novel intravenous injectable TLR7 agonist, DSP-0509, synergistically enhanced antitumor immune responses in combination with anti-PD-1 antibody [Abstract 4726]. Cancer Res. 2018. doi:10.1158/1538-7445.AM2018-4726.
- Du B, Jiang Q, Cleveland J, Liu B, Zhang D. Targeting toll-like receptors against cancer. J Cancer Metastasis Treat. 2016;2:463-470.
- Chi H, Li C, Zhao FS, et al. Anti-tumor activity of toll-like receptor 7 agonists. Front Pharmacol. 2017;8:304: doi:10.3389/fphar.2017.00304.
- Peterson P, Kim W, Haws H, et al. The ALK-2 inhibitor, TP-0184, demonstrates high distribution to the liver contributing to significant preclinical efficacy in mouse models of anemia of chronic disease [Abstract]. Blood. 2016;128:263.
- Peterson P, Whatcott C, Siddiqui-Jain A, et al. TP-0184 inhibits ALK2/ACVR1, decreases hepcidin levels, and demonstrates activity in preclinical mouse models of functional iron deficiency. Blood. 2017;13(suppl 1):937.
- Buczkowicz P, Hoeman C, Rakopoulos P, et al. Genomic analysis of diffuse intrinsic pontine gliomas identifies three molecular subgroups and recurrent activating ACVR1. Nat Genet. 2014;46(5):451-456.
- Taylor K, Mackay A, Truffaux N, et al. Recurrent activating ACVR1 mutations in diffuse intrinsic pontine glioma. Nat Genet. 2014;46(5):457-461.
- Zhao B, Pritchard J. Inherited disease genetics improves the identification of cancer-associated genes. PLOS Genet. 2016;12(6):e1006081.
- Peterson P, Soh KK, Lee YS, et al. ALK2 inhibition via TP-0184 abrogates inflammation-induced hepcidin expression and is a potential therapeutic for anemia of chronic disease [Abstract]. Blood. 2015;126:273.
- Tolero Pharmaceuticals Inc. Data on file.
- Kim W, Haws H, Peterson P, et al. TP-1287, an oral prodrug of the cyclin-dependent kinase-9 inhibitor alvocidib [Abstract 5133]. Cancer Res. 2017;77(13 suppl). doi:10.1158/1538-7445.AM2017-5133.
- Huang H, Weng H, Zhou H, Qu L. Attacking c-Myc: targeted and combined therapies for cancer. Curr Pharm Des. 2014;20(42):6543-6554. doi:10.2174/1381612820666140826153203.
- George B, Richards D, Edenfield W, et al. A phase I, first-in-human, open-label, dose escalation, safety, pharmacokinetic, and pharmacodynamic study of oral TP-1287 administered daily to patients with advanced solid tumors. Poster presented at: ASCO 2020; May 29-31, 2020; Digital.
- Foulks JM, Carpenter KJ, Luo B, et al. A small-molecule inhibitor of PIM kinases as a potential treatment for urothelial carcinomas. Neoplasia. 2014;16(5):403-412.
- Zhang X, Song M, Kundu JK, Lee M, Liu ZZ. PIM kinase as an executional target in cancer. J Cancer Prev. 2018;23:109-116.
- Garrido-Laguna I, Dillon P, Anthony S, et al. A phase I, first-in-human, open-label, dose escalation, safety, pharmacokinetic, and pharmacodynamic study or oral TP-3654 administered daily for 28 days to patients with advanced solid tumors. Poster presented at: ASCO 2020; May 29-31; Digital.
- Pathi S, Peterson P, Mangelson R, et al. PKM2 activation modulates metabolism and enhances immune response in solid tumor models [Abstract B080]. Mol Can Ther. 2019. doi:10.1158/1535-7163.TARG-19-B080.
- Zahra K, Dey T, Ashish, Mishra SP, Pandey U. Pyruvate kinase M2 and cancer: the role of PKM2 in promoting tumorigenesis. Front Oncol. 2020;10:159. doi:103389/fonc.2020.00159.
- He X, Du S, Lei T, et al. PKM2 in carcinogenesis and oncotherapy. Oncotarget. 2017;8(66):110656-110670.