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Welcome to DDRiver Clinical Trial Program

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OUR PROGRAM

Welcome to the DDRiverTM Clinical Trials Program—a program investigating the anticancer effect of inhibiting the DNA damage response (DDR) pathway in multiple tumor types.

Several DDR inhibitors are under clinical investigation and have not been proven to be safe and effective. There is no guarantee that any compound will be approved in the sought-after indication by any health authority worldwide.


Find out more about our programs below

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Every cell in the human body is subject to DNA damage. If that damage is not properly repaired, changes to DNA can be passed on to daughter cells, and the resulting mutations can promote the development of cancer.1,2 Normal cells have mechanisms, collectively known as the DNA damage response (DDR), to detect and repair DNA damage or induce cell death if the damage cannot be fixed.3 Many cancers have defects in DDR proteins and pathways that may render cells more susceptible to DNA damage.3,4

In cancer cells, inhibitors of the DDR have the potential to prevent DNA repair or maximize DNA damage that is caused by anticancer therapies, ultimately resulting in cancer cell death. Additionally, in tumors that have acquired mutations in one or more DDR pathways, rendering them nonfunctional, inhibition of the remaining DDR pathway(s) could be fatal to cancer cells.3-5

Berzosertib (M6620)

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Berzosertib is an investigational intravenously administered inhibitor of
ataxia telangiectasia and Rad3-related (ATR) protein kinase6,7

M1774

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M1774 is an investigational orally administered inhibitor of ataxia telangiectasia and Rad3-related (ATR) protein kinase8,9

M4076

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M4076 is an investigational orally administered ATP-competitive inhibitor of ataxia telangiectasia mutated (ATM) protein kinase10

Peposertib (M3814)

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Peposertib is an investigational orally administered inhibitor of
DNA-dependent protein kinase (DNA-PK)11,12

References
1. Tubbs A, Nussenzweig A. Cell. 2017;168:644–656; 2. Chin CF, Yeong FM. Mol Cell Biol. 2010;30:22–32; 3. Blackford N, Jackson P. Mol Cell. 2017;66:801–817; 4. Ford JM, Kastan MB. DNA damage response pathways. In: Abeloff's Clinical Oncology. Publisher: Elsevier. 2019:154–164; 5. Minten EV, Yu DS. Clin Oncol (R Coll Radiol). 2019;31:303–310; 6. Yap TA, et al. J Clin Oncol. 2020;38:3195–3204; 7. ClinicalTrials.gov. Accessed February 24, 2021. https://clinicaltrials.gov/ct2/show/NCT04768296; 8. Roidos P, et al. Nat Commun. 2020;11(1):4077. 9. ClinicalTrials.gov. Accessed February 24, 2021. https://clinicaltrials.gov/ct2/show/NCT04170153; 10. Fuchss T, et al. AACR 2019. Poster 3500; 11. Zenke FT, et al. Mol Cancer Ther. 2020;19(5)1091-1101; 12. ClinicalTrials.gov. Accessed February 24, 2021. https://clinicaltrials.gov/ct2/show/NCT03770689.