VENTANA® MMR RxDx Panel

IVD For in vitro diagnostic use.

US FDA

Driving diagnostic certainty for life-changing decisions in solid tumors

The VENTANA MMR RxDx Panel is the first FDA-approved immunohistochemistry (IHC) assay to identify patients with:1,2

  • MMR-deficient (dMMR) solid tumors, including endometrial carcinoma, eligible for treatment with JEMPERLI® (dostarlimab-gxly) or KEYTRUDA® (pembrolizumab)
  • MMR-proficient (pMMR) endometrial carcinoma, eligible for combination therapy with KEYTRUDA® (pembrolizumab) and LENVIMA® (lenvatinib)
  • MMR-deficient (dMMR) endometrial carcinoma, eligible for treatment with IMFINZI® (durvalumab)

It is estimated that up to 4% of all solid tumors are dMMR.3 Cancer continues to be a significant societal challenge as the second leading cause of death in the United States and worldwide.4 In the US, the vast majority of new cases will consist of solid tumors, approximately 16% of which will have been shown to have defects in any of the MMR proteins. Patients with dMMR solid tumors that have progressed on or following prior treatment and have no other options are now eligible for these therapies.5

Benefits at a glance

Benefits at a glance

CE IVD

Driving diagnostic certainty for life-changing decisions in multiple cancers

The VENTANA MMR RxDx Panel is the first IVDR-approved immunohistochemistry (IHC) assay to identify patients with:1,2

  • MMR-deficient (dMMR) endometrial carcinoma eligible for treatment with JEMPERLI® (dostarlimab-gxly)
  • MMR-deficient (dMMR) colorectal (CRC), endometrial, gastric, biliary, or small intestine cancer eligible for treatment with KEYTRUDA® (pembrolizumab)
  • MMR-deficient (dMMR) endometrial carcinoma eligible for treatment with IMFINZI® (durvalumab)
  • MMR-proficient (pMMR) endometrial carcinoma eligible for treatment IMFINZI® (durvalumab) + LYNPARZA® (olaparib)

Cancer is the second leading cause of death worldwide, with nearly 10 million deaths annually.3 High microsatellite instability (MSI-H) and dMMR has been reported in 20-40% of endometrial cancers (one of many solid tumor types).4-6 While the treatment of each disease varies, evaluation of the MMR status of solid tumors is helpful for prognosis and guiding treatment.7

Benefits at a glance

Benefits at a glance

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Panel interpretation

A loss of expression of any of the essential MMR proteins, including MLH1, PMS2, MSH2, or MSH6, in the presence of evaluable internal controls causes MMR deficiency. Presence of staining for all four MMR protein markers in the tumor in the presence of evaluable internal controls indicates that the case is proficient for mismatch repair status. Absence of staining in any one of the MMR protein markers of VENTANA MMR RxDx Panel indicates a case is deficient for mismatch repair status.

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Training and educational resources for pathologists

Explore educational content on biomarkers and disease areas, interactive interpretation training, scoring guidance and case reviews—designed to advance your knowledge and support greater proficiency with VENTANA companion diagnostic assays.

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Do you have questions about our products or services? We’re here to help. Contact a Roche representative in your region.

US FDA references

  1. F. Hoffmann-La Roche Ltd. IHC Menu. 2025.
  2. F. Hoffmann-La Roche Ltd. VENTANA MMR RxDx Panel Package Inserts. 2026.
  3. Lorenzi M, Amonkar M, Zhang J, et. al. Epidemiology of Microsatellite Instability High (MSI-H) and Deficient Mismatch Repair(dMMR)in Solid Tumors: A Structured Literature Review. J. Oncology. 2020; (22):1-17.
  4. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2020. CA Cancer J Clin. 2020:70(1):7-30.
  5. Le DT, Durham JN, Smith KN, et al. Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade. Science. 2017;357(6349):409-413.
  6. Yamashita H, Nakayama K, Ishikawa M, et al. Microsatellite instability is a biomarker for immune checkpoint inhibitors in endometrial cancer. Oncotarget. 2017;9(5):5652-5664.
  7. Xiao X, Dong D, He W, et al. Mismatch repair deficiency is associated with MSI phenotype, increased tumor-infiltrating lymphocytes and PD-L1 expression in immune cells in ovarian cancer. Gynecol Oncol. 2018;149(1):146-154
  8. Sloan EA, Ring KL, Willis BC, et al. PD-L1 expression in mismatch repair-deficient endometrial carcinomas, including Lynch syndrome-associated and MLH1 promoterhypermethylated tumors. Am J Surg Pathol. 2017;41(3):326-333.
  9. Dudley JC, Lin MT, Le DT, et al. Microsatellite instability as a biomarker for PD-1 blockade. Clin Cancer Res. 2016;22(4):813-820.

CE IVD references

  1. F. Hoffmann-La Roche Ltd. IHC Menu. 2025.
  2. F. Hoffmann-La Roche Ltd. VENTANA MMR RxDx Panel Package Inserts. 2026.
  3. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019;69(1):7-34.
  4. Kato M, et al. DNA mismatch repair-related protein loss as a prognostic factor in endometrial cancers. J Gynecol Oncol. 2015;26(1):40-5. 
  5. Matthews KS, et al. Lynch syndrome in women less than 50 years of age with endometrial cancer. Obstet Gynecol. 2008;111(5):1161-6.
  6. Kim SR, et al. Does MMR status in endometrial cancer influence response to adjuvant therapy? Gynecol Oncol. 2018;151(1):76-81.
  7. Tran AQ and Gehrig P. Recent advances in endometrial cancer. F1000Res. 2017;6:81-90. 
  8. Le DT, et al. Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade. Science. 2017;357(6349):409-13.
  9. Yamashita H, et al. Microsatellite instability is a biomarker for immune checkpoint inhibitors in endometrial cancer. Oncotarget. 2017;9(5):5652-64.
  10. Xiao X, et al. Mismatch repair deficiency is associated with MSI phenotype, increased tumor-infiltrating lymphocytes and PD-L1 expression in immune cells in ovarian cancer. Gynecol Oncol. 2018;149(1):146-54.
  11. Sloan EA, et al. PD-L1 expression in mismatch repair-deficient endometrial carcinomas, including Lynch syndrome-associated and MLH1 promoter hypermethylated tumors. Am J Surg Pathol. 2017;41(3):326-33. 
  12. Dudley JC, et al. Microsatellite instability as a biomarker for PD-1 blockade. Clin Cancer Res. 2016;22(4):813-20.