On April 7, 2017 Hutchison China MediTech Limited ("Chi-Med") (AIM/Nasdaq: HCM) reported pre-clinical data for fruquintinib and sulfatinib at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) ("AACR") Annual Meeting 2017, held in Washington, D.C., USA from April 1 to 5, 2017 (Press release, Hutchison China MediTech, APR 7, 2017, http://www.chi-med.com/pre-clinical-data-at-aacr-2017/ [SID1234518510]). Fruquintinib and sulfatinib are both being evaluated in Phase III clinical trials for various cancers.

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Fruquintinib is designed to be a highly selective and potent oral inhibitor of vascular endothelial growth factor receptors ("VEGFR") with a tolerability profile that enables rational combination with other cancer therapies. A new drug application ("NDA") for fruquintinib to the China Food and Drug Administration ("CFDA") is expected to be filed in mid-2017. It is currently under the joint development in China by Chi-Med and its partner Eli Lilly and Company ("Lilly").

Sulfatinib is an oral, novel angio-immunokinase inhibitor that selectively targets VEGFR, fibroblast growth factor receptor ("FGFR") and colony-stimulating factor-1 receptor ("CSF 1R"), three key tyrosine kinase receptors involved in tumor angiogenesis and immune evasion. Two Phase III trials are underway in neuroendocrine tumor ("NET") patients in China.

The presentations were as follows:

Presentation Title: Evaluation of fruquintinib, a potent and selective oral VEGFR inhibitor, in combination with targeted therapies or immune checkpoint inhibitors in preclinical tumor models

Authors: Yongxin Ren et al.

Abstract: #2089

Session: Growth Factor and Hormone Receptors as Therapeutic Targets

Date & Time: Monday, April 3, 2017, 1:00 PM (EST)

Presentation Title: Preclinical evaluation of sulfatinib, a novel angio-immuno kinase inhibitor targeting VEGFR, FGFR1 and CSF-1R kinases

Authors: Jinghong Zhou et al.

Abstract: #4187

Session: Targeting Protein Kinases and DNA Repair

Date & Time: Tuesday, April 4, 2017, 1:00 PM (EST)

The presentations are available at www.chi-med.com/news/. Further information about AACR (Free AACR Whitepaper) is available at aacr.org.


ABSTRACTS
Evaluation of fruquintinib, a potent and selective oral VEGFR inhibitor, in combination with targeted therapies or immune checkpoint inhibitors in preclinical tumor models

Authors: Yongxin Ren, Qiaoling Sun, Jingwen Long, Shiming Fan, Renxiang Tang, Wei Zhang, Xuelei Ge, Jianxing Tang, Linfang Wang, Dongxia Shi, Hongbo Chen, Min Cheng, Weiguo Qing and Weiguo Su

The development of therapies targeting tumor angiogenesis, tumor driver gene alterations and tumor immune evasion has made tremendous advancement in improving overall survival ("OS"). However, efficacy may be limited and resistance often develops rapidly when targeting a single axis of tumorigenesis. Therefore, it is worthwhile to explore rational combination of therapies based on tumor-specific features. Fruquintinib is a potent and selective oral VEGFR inhibitor currently in Phase III clinical trials for non-small-cell lung cancer ("NSCLC") and colorectal cancer ("CRC"). We report here the evaluation of anti-tumor effect of fruquintinib in preclinical animal tumor models in combination with therapies targeting tumor driver gene alterations such as epidermal growth factor receptor ("EGFR") and mesenchymal growth factor receptor ("c-MET") or with immune checkpoints.

In NSCLC xenograft models with EGFR activation such as activating mutations, gene amplification or protein overexpression, fruquintinib plus an EGFR tyrosine kinase inhibitor such as gefitinib or theliatinib (HMPL-309) was found to be more efficacious than either monotherapy. For instance, in PC-9 subcutaneous tumor model carrying EGFR exon 19 deletion, single agent treatment with fruquintinib at 2 mg/kg and gefitinib at 5 mg/kg produced the tumor growth inhibition ("TGI") of 58% and 63%, respectively, while the combination treatment resulted in a TGI of 100% and tumor regression was observed in 11 of 16 mice treated with combinational therapy. In multiple xenograft models derived from lung cancer or renal cell cancer with c-MET activation (amplification or over-expression), addition of fruquintinib to a c-MET inhibitor savolitinib (AZD6094, HMPL-504) also improved the tumor growth inhibition substantially. At the end of the efficacy studies, CD31 and phosphorylation of EGFR, c-MET, protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) were analyzed with immunohistochemistry and western blotting method in tumor tissues. The results suggested that the enhanced anti-tumor effect in combination therapy could be attributed to the simultaneous blockade of cell signaling in tumor cells (EGFR or c-MET) and VEGFR suppression in the tumor microenvironment.

Up-regulation of the immune inhibitory checkpoints induced by vascular endothelial growth factor ("VEGF") is one of the important mechanisms for tumor cells to escape immune surveillance. In a syngeneic murine tumor model, co-administration of fruquintinib and anti-Programmed death-ligand 1 ("PD-L1") antibody was found to provide improved anti-tumor effect compared to fruquintinib or anti-PD-L1 single agent alone. Studies to understand the mechanism responsible for the combination effect are underway.

All combinations with fruquintinib described above were well tolerated. The efficacy observed in these models suggested that simultaneous blockade of tumor angiogenesis and tumor cell signaling or immune evasion may be a promising approach in improving treatment outcomes.

Preclinical evaluation of sulfatinib, a novel angio-immuno kinase inhibitor targeting VEGFR, FGFR1 and CSF-1R kinases

Authors: Jinghong Zhou, Jun Ni, Min Cheng, Na Yang, Junqing Liang, Liang Ge, Wei Zhang, Jianxing Tang, Qiaoling Sun, Fu Li, Jia Hu, Dongxia Shi, Hongbo Chen, Jingwen Long, Junen Sun, Fang Yin, Xuelei Ge, Hong Jia, Feng Zhou, Yongxin Ren, Weiguo Qing and Weiguo Su

Both VEGFR and FGFR signaling pathways can mediate tumor angiogenesis. CSF-1R plays an important role on functions of macrophages. Recently, the roles in increasing tumor immune evasion of VEGFR, FGFR in regulation of T cells, tumor-associated macrophages ("TAMs") and myeloid-derived suppressor cells have been demonstrated. Therefore, blockade of tumor angiogenesis and tumor immune evasion by simultaneously targeting VEGFR, FGFR and CSF-1R kinases may represent a promising approach for anti-cancer therapy.

We report here the preclinical studies for sulfatinib (HMPL-012), a potent and highly selective small molecule tyrosine kinase inhibitor against VEGFR, FGFR1 and CSF-1R. Sulfatinib inhibited VEGFR1, 2, and 3, FGFR1 and CSF-1R kinases with IC50s in a range of 1~24 nM, and it strongly blocked VEGF induced VEGFR2 phosphorylation in HEK293KDR cells and colony-stimulating factor-1 stimulated CSF-1R phosphorylation in RAW264.7 cells with IC50 of 2 and 79 nM, respectively. Sulfatinib also attenuated VEGF or FGF stimulated HUVEC cells proliferation with IC50 < 50 nM. In animal studies, a single oral dosing of sulfatinib inhibited VEGF stimulated VEGFR2 phosphorylation in lung tissues of nude mice in an exposure-dependent manner. Furthermore, elevation of FGF23 levels in plasma 24 hours post dosing suggested suppression of FGFR signaling. Sulfatinib demonstrated potent tumor growth inhibition in multiple human xenograft models and decreased CD31 expression remarkably, suggesting strong inhibition on angiogenesis through VEGFR and FGFR signaling. In a syngeneic murine colon cancer model CT-26, sulfatinib demonstrated moderate tumor growth inhibition after single agent treatment. Flow cytometry and immunohistochemistry analysis revealed an increase of CD8+ T cells and a significant reduction in TAMs, (CD163+ or F4/80+CD11b+CD45+) and CSF-1R+ TAMs in tumor tissue indicating strong effect on CSF-1R. Interestingly, combination of sulfatinib with a PD-L1 antibody resulted in enhanced anti-tumor effect. These results suggested that sulfatinib has a strong effect in modulating angiogenesis and cancer immunity.

In summary, sulfatinib is a novel angio-immuno kinase inhibitor targeting VEGFR, FGFR1 and CSF-1R kinases that could simultaneously block tumor angiogenesis and immune evasion. This unique feature seems to support sulfatinib as an attractive candidate for exploration of possible combinations with checkpoint inhibitors against various cancers. Sulfatinib is currently in multiple clinical trials including two Phase III trials against neuroendocrine tumors.

About Fruquintinib
Fruquintinib is a highly selective small molecule drug candidate that has been shown to inhibit VEGFR 24 hours a day via an oral dose, without known off-target toxicities. At an advanced stage, tumors secrete large amounts of VEGF, a protein ligand, to stimulate formation of excessive vasculature (angiogenesis) around the tumor to provide greater blood flow, oxygen, and nutrients to the tumor. VEGF and VEGFR play a pivotal role in tumor-related angiogenesis, and the inhibition of the VEGF/VEGFR pathway. This represents an important therapeutic strategy in blocking the development of new blood vessels essential for tumors to grow and invade.

Fruquintinib is currently under joint development in China by Chi-Med and its partner Lilly. In early March, Chi-Med and Lilly jointly announced top-line results from FRESCO, the Phase III pivotal registration trial of fruquintinib in 416 patients with locally advanced or metastatic CRC in China, who failed at least two prior chemotherapies, including fluoropyrimidine, oxaliplatin and irinotecan. The FRESCO trial met its primary endpoint of demonstrating a clinically meaningful and a statistically significant increase in OS in the intention-to-treat ("ITT") population of patients treated with fruquintinib plus best supportive care ("BSC") as compared to patients treated with placebo plus BSC. Chi-Med is currently preparing to submit an NDA for fruquintinib to the CFDA. In addition to OS, a statistically significant improvement in progression-free survival ("PFS"), a key secondary endpoint, was observed. The adverse events demonstrated in FRESCO did not identify any new or unexpected safety issues. Full detailed results are subject to ongoing analysis and are expected to be disclosed at an upcoming scientific meeting in mid-2017.

In addition to the FRESCO CRC trial, fruquintinib is being studied in China in a Phase III pivotal trial in NSCLC, known as FALUCA; and a Phase II study using fruquintinib combined with Iressa (gefitinib) in the first-line setting for patients with advanced or metastatic NSCLC. Other studies currently being planned, and soon to be initiated, include a Phase III study in gastric cancer in combination with paclitaxel in China, new studies in the United States, and certain exploratory studies in combination with other oncology agents.

About Sulfatinib
Sulfatinib is an oral, novel angio-immunokinase inhibitor that selectively inhibits the tyrosine kinase activity associated with VEGFR, FGFR and CSF-1R, three key tyrosine kinase receptors involved in tumor angiogenesis and immune evasion. Inhibition of the VEGFR signaling pathway can act to stop angiogenesis, the growth of the vasculature around the tumor, and thereby starve the tumor of the nutrients and oxygen it needs to grow rapidly. Aberrant activation of the FGFR signaling pathway, which can be increased by anti-VEGFR therapy treatment, is shown to be associated with cancer progression by promoting tumor growth, angiogenesis and formation of the myeloid derived suppressor cells. Inhibition of the CSF-1R signaling pathway blocks the activation of tumor-associated macrophages, which are involved in suppressing immune responses against tumors.

Six sulfatinib clinical trials are underway in China and the United States, including two Phase III studies and one Phase II study in NET patients (SANET-p, SANET-ep and SANET-1), one Phase II study in thyroid cancer patients and one Phase II study in biliary tract cancer patients.

On April 7, 2017 Kura Oncology, Inc. (NASDAQ:KURA), a clinical stage biopharmaceutical company focused on the development of precision medicines for oncology, reported that the first patient has been dosed in its Phase 1 clinical trial of KO-947, a potent and selective small molecule inhibitor of extracellular-signal-regulated kinases 1 and 2 (ERK1/2) (Press release, Kura Oncology, APR 7, 2017, View Source [SID1234518509]).

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"We are committed to the discovery and development of product candidates that target oncogenes and oncogenic pathways for the treatment of cancer," said Troy Wilson, Ph.D., J.D., President and CEO of Kura. "We believe KO-947 holds much promise as a potential therapeutic, and its advancement into the clinic underscores Kura’s productivity and commitment to building a diverse pipeline of precision medicines."

"The RAS/RAF/MEK/ERK pathway is dysregulated in more than 30% of human cancers, including tumors arising from mutations in KRAS, NRAS and BRAF, encompassing a number of cancer indications with significant unmet medical need," said Antonio Gualberto, M.D., Ph.D., Chief Medical Officer of Kura. "We believe the unique and differentiated drug properties of KO-947, as well as a significant body of preclinical data including data just presented at the AACR (Free AACR Whitepaper) meeting this week, make it a compelling therapeutic candidate, and we look forward to evaluating its tolerability and activity in the clinic."

The Phase 1 trial of KO-947 is designed to determine the maximum tolerated dose of KO-947 in patients with locally advanced unresectable or metastatic, relapsed and/or refractory, non-hematological malignancies. The trial design includes a dose escalation, maximum–tolerated dose expansion and one or more tumor-specific extension cohorts. Currently, two tumor-specific cohorts, non-small cell lung cancer with mutations in RAS or BRAF and squamous cell carcinomas, have been identified as potential extension cohorts. Additional information about this clinical trial is available at clinicaltrials.gov using the identifier: NCT03051035

About KO-947

KO-947 is a potent and selective small molecule inhibitor of ERK1/2 kinases. KO-947 exhibits potent anti-proliferative activity across a broad panel of tumor cell lines with mutations in BRAF, NRAS or KRAS and demonstrates prolonged pathway inhibition, both in vitro and in vivo. Durable tumor regression has been observed with KO-947 in preclinical cell line and patient derived xenograft models, including KRAS- and BRAF-mutant adenocarcinomas and squamous cell carcinomas lacking BRAF/RAS mutations.

On April 7, 2017 Kyowa Hakko Kirin Co., Ltd. (Tokyo: 4151, President and CEO: Nobuo Hanai, "Kyowa Hakko Kirin") reported the Global Phase 3 study (MAVORIC: Mogamulizumab anti-CCR4 Antibody Versus ComparatOR In CTCL) investigating the use of mogamulizumab (KW-0761) in patients with cutaneous T-cell lymphoma (CTCL) met its primary endpoint of progression free survival (Press release, Kyowa Hakko Kirin, APR 7, 2017, View Source [SID1234518503]).

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MAVORIC is a Phase 3 Open-Label, Multi-Center, Randomized Study of mogamulizumab versus vorinostat in patients with CTCL who have failed at least one prior systemic treatment. The study is conducted in the US, Europe, Japan and Australia, and randomized 372 patients to receive either mogamulizumab or vorinostat. The top-line results demonstrated a statistically significant improvement in progression free survival in the mogamulizumab arm compared to the control (vorinostat) arm, and tolerable safety profile of mogamulizumab.

Kyowa Hakko Kirin will complete a full evaluation of the data from the MAVORIC study and work with investigators on the future presentation and publication of results. Kyowa Hakko Kirin plans to initiate discussions with global regulatory authorities in 2017 about plans for pursuing marketing authorizations for mogamulizumab in CTCL.

"We are delighted with the positive results from the MAVORIC study which is the largest, global randomized phase 3 clinical study ever conducted in patients with CTCL." said Mitsuo Satoh, Executive Officer, Vice President, Head of Research and Development Division of Kyowa Hakko Kirin.
"We look forward to reviewing the data with regulatory agencies in the near future." said Stephen Letrent, Pharm.D, Ph.D, Senior Vice President, Kyowa Kirin Pharmaceutical Development.

The Kyowa Hakko Kirin Group companies strive to contribute to the health and well-being of people around the world by creating new value through the pursuit of advances in life sciences and technologies.

About Mogamulizumab
Mogamulizumab is a humanized monoclonal antibody (mAb) directed against CC chemokine receptor 4 (CCR4), which is frequently expressed on leukemic cells of certain hematologic malignancies including CTCL. Mogamulizumab was produced using Kyowa Hakko Kirin’s proprietary POTELLIGENT platform, which is associated with enhanced antibody-dependent cellular cytotoxicity (ADCC). Mogamulizumab was first granted marketing authorization in Japan in March 2012 for the treatment of patients with relapsed or refractory CCR4-positive Adult T-cell Leukemia-Lymphoma (ATL) under the trade name POTELIGEO. The drug was subsequently granted marketing authorization in Japan for the treatment of patients with relapsed or refractory CCR4-positive, peripheral T-cell lymphoma (PTCL) and CTCL in March 2014, and with chemotherapy-naive CCR4-positive ATL in December 2014.

About Cutaneous T-cell Lymphoma (CTCL)
CTCL is a rare type of non-Hodgkin’s lymphoma which is characterized by localization of malignant T lymphocytes to the skin. The two most common types of CTCL are mycosis fungoides (MF) and Sézary syndrome (SS), and depending on the stage, the disease may involve skin, blood, lymph nodes, viscera and other organs.

On April 6, 2017 Innocrin Pharmaceuticals, Inc., a clinical-stage company focused on the development of the oral, selective CYP17-lyase/androgen receptor (AR) inhibitor, seviteronel, reported the appointment of Fred Eshelman, PharmD, of Eshelman Ventures as Chief Executive Officer, effective March 15, 2017 (Press release, Innocrin Pharmaceutical, APR 6, 2017, View Source [SID1234518507]).


Douglas Reed, MD, Innocrin Chairman of the Board stated, "I am pleased to have Fred lead the Innocrin team as the company enters mid-stage clinical development for breast and prostate cancer. His transactional and drug development expertise will serve Innocrin well as the company and its clinical programs continue to mature."

Fred Eshelman is the founder of Eshelman Ventures LLC, an investment company primarily interested in private healthcare companies. Previously he founded and served as CEO and Executive Chairman of Pharmaceutical Product Development (NASDAQ: PPD). After PPD he served as Founding Chairman and largest shareholder of Furiex Pharmaceuticals (NASDAQ: FURX), which was sold to Forest Labs/Actavis in July, 2014. His career has also included positions as senior vice president of development and board member of the former Glaxo, Inc., as well as various management positions with Beecham Laboratories and Boehringer Mannheim Pharmaceuticals.

"As the lead investor of Innocrin’s last round of financing, I am fully committed to the success of the seviteronel clinical development programs, since the drug provides novel treatment options for breast and prostate cancer sub-types where patients have failed other therapies. I am not only investing in seviteronel, but also betting on members of the development team as I join the company’s day-to-day leadership," said Dr. Eshelman.

Innocrin also announced that the FDA granted a second Fast Track Designation for seviteronel (VT-464). The new designation is for the treatment of women with advanced AR+ triple-negative breast cancer (TNBC) and women or men with advanced estrogen receptor-positive (ER+) breast cancer.

Established under the FDA Modernization Act of 1997, the Fast Track program is designed to facilitate the development and review of drugs intended to treat serious conditions and fill an unmet medical need. A drug development program with Fast Track designation is afforded greater access to FDA for the purpose of expediting the drug’s development, review and potential approval.

"We believe that the award of a second Fast Track designation for seviteronel, in addition to men with castration resistant prostate cancer (CRPC), is continued FDA recognition of the compound’s potential to address significant unmet medical need in hormone-dependent cancers," stated Dr. Eshelman.

Edwina Baskin-Bey, M.D. Innocrin Chief Medical Officer stated, "Granting of the FDA Fast Track Designation for seviteronel treatment of women and men with advanced breast cancer helps to accelerate our already aggressive clinical development programs. Increased FDA collaborations and rolling reviews for both CRPC and breast cancer will allow for us to continue our momentum of bringing seviteronel to patients in need of new treatment options."

Innocrin also announced that it recently completed enrollment of women with ER+ breast cancer in the Phase 2 CLARITY (CYP17 Lyase and Androgen Receptor Inhibitor Treatment with Seviteronel) study (INO-VT-464-006; NCT02580448) and enrollment of women with TNBC and men with ER+ breast cancer is ongoing. Phase 2 enrollment in its prostate cancer studies are also ongoing in men who have progressed following abiraterone, enzalutamide or both.

Innocrin also announced presentations at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) annual meeting (1-5 April 2017) and the upcoming American Urological Association (AUA) annual meeting (12-16 May 2017) describing new combination and single-agent seviteronel results in breast and prostate models resistant to approved therapies. Updated Phase 2 breast cancer clinical results will be presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting (2-6 June 2017).

About Seviteronel (VT-464)

Seviteronel is a once-daily oral therapeutic given without prednisone. Seviteronel selectively inhibits CYP17 lyase, an enzyme needed for the synthesis of androgens and estrogens, and also directly blocks the AR.

It is thought that the AR may stimulate disease progression of breast cancer tumors that no longer are ER+ (e.g., are triple-negative) or are ER+ but have become resistant to ER-directed therapies such as aromatase inhibitors or tamoxifen. Preclinical study results presented at the 2015 San Antonio Breast Cancer Symposium, confirmed that seviteronel, due to its multiple mechanisms of action, blocks the growth of resistant ER+ and AR+ breast cancer cells more potently than enzalutamide. Phase 2 enrollment of women and men with breast cancer is ongoing in the CLARITY-01 (CYP17 Lyase and Androgen Receptor Inhibitor Treatment with Seviteronel) study (NCT02580448).

A growing body of preclinical and clinical evidence shows that seviteronel blocks the growth of deadly CRPC that is resistant to abiraterone (a CYP17 hydroxylase inhibitor) or enzalutamide (an AR antagonist). CRPC disease progression following treatment with abiraterone, enzalutamide or both represents a major unmet medical need due to the widespread and growing use of both agents, as well as the high cross-resistance between these agents (e.g., cancers that are resistant to abiraterone are typically resistant to enzalutamide and vice versa). Fast Track Designation was granted for seviteronel treatment of men with CRPC 10 December 2015. Enrollment is ongoing in two Phase 2 studies (NCT02012920, NCT02445976).

About Breast Cancer

Each year over 230,000 women and 2,300 men are diagnosed with breast cancer in the United States, with almost 40,000 and 440 deaths attributable to the disease. While estrogen deprivation is currently the standard of care for ER+ BCa, the majority of patients eventually develop resistance. ER+ patients comprise ~75% of all metastatic breast cancer cases, and TNBC accounts for ~15-20%. TNBC has a more aggressive course than ER+ BCa does but both have poor survival rates post-failure of endocrine and/or chemotherapy.

About Prostate Cancer

Prostate cancer is the second most common form of cancer affecting men in the United States: an estimated one in six will be diagnosed with prostate cancer in his lifetime. Prostate cancer afflicts nearly 240,000 men each year in the US and approximately 36,000 men die due to metastatic CRPC.

On April 6, 2017 Myriad Genetics, Inc. (NASDAQ:MYGN), a leader in molecular diagnostics and personalized medicine, reported that it has entered into a companion diagnostic development collaboration with BeiGene, a clinical-stage biopharmaceutical company developing molecularly-targeted and immuno-oncology drugs for the treatment of cancer, to accelerate precision medicine in oncology (Press release, Myriad Genetics, APR 6, 2017, View Source [SID1234518501]).

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Under the agreement, BeiGene will use Myriad’s myChoice HRD and BRACAnalysis CDx companion diagnostic tests to support the clinical development of its novel PARP inhibitor, BGB-290. Specific terms of the deal were not disclosed.

"We are excited to collaborate with BeiGene to help identify patients who stand to benefit the most from treatment with BGB-290," said Mark C. Capone, president and CEO, Myriad Genetics. "As the pioneer in companion diagnostics for PARP inhibitors, we recognize that precision medicine only can be achieved by molecularly matching patients to the right therapy. Together with BeiGene, we are in a unique position to integrate advanced genetic information into clinical practice and achieve better patient outcomes."

About BRACAnalysis CDx
BRACAnalysis CDx is an in vitro diagnostic device intended for the qualitative detection and classification of variants in the protein coding regions and intron/exon boundaries of the BRCA1 and BRCA2 genes using genomic DNA obtained from whole blood specimens.

About myChoice HRD
Myriad’s myChoice HRD is the first homologous recombination deficiency test that can detect when a tumor has lost the ability to repair double-stranded DNA breaks, resulting in increased susceptibility to DNA-damaging drugs such as platinum drugs or PARP inhibitors. It is estimated that 1.8 million people in the United States and Europe who are diagnosed with cancers annually may be candidates for treatment with DNA-damaging agents.