Medivir invites to a conference call today on updated data at ASCO GI and the plans moving forward for fostrox in primary liver cancer (HCC)

On January 23, 2024 Medivir AB (Nasdaq Stockholm: MVIR), a pharmaceutical company focused on developing innovative treatments for cancer in areas of high unmet medical need, reported invite to a conference call on the updated data from the ongoing phase 1b/2a study in advanced hepatocellular carcinoma (HCC) (Press release, Medivir, JAN 23, 2024, View Source [SID1234639440]). The data was presented at the ASCO (Free ASCO Whitepaper) (American Society of Clinical Oncology) GI (Gastrointestinal Cancers) Symposium in San Francisco on January 19. The conference call will be held today January 23, at 14.00 CET, to update on the results in the study and the plans moving forward, including feedback from extensive interactions with world renowned experts at the ASCO (Free ASCO Whitepaper) GI congress.

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The data (poster number 476P) from the ongoing fostrox + Lenvima study, presented on Friday January 19 by Dr Maria Reig from Hospital Clinic of Barcelona in Spain, showed that fostrox + Lenvima remains tolerable, with no new, unexpected safety events and that the clinical benefit continues to improve further, as the study progresses and data matures.

– "The updated study results presented at ASCO (Free ASCO Whitepaper) GI has further strengthened our belief in the combination of fostrox + Lenvima as a potential treatment for patients with advanced HCC. The conference also enabled extensive interactions with global experts in HCC which provided important input regarding the design of our upcoming study. Expert guidance is of particular value when preparing for interactions with regulatory authorities to discuss final study design of the planned, registrational phase 2b study with accelerated approval intent," says Dr. Pia Baumann, CMO at Medivir.

Conference call for investors, analysts and the media

Presenters from Medivir: Jens Lindberg, CEO, Pia Baumann, CMO and Fredrik Öberg, CSO.

Time: Tuesday January 23, 2024, at 14.00 CET

To access the webcast and information about the teleconference, please click HERE!

The webcast will also be streamed via a link on the website: www.medivir.com/investors/calendar

The presentation will be available on Medivir’s website after the conference call.

The poster will also be available on Medivir’s website.

For additional information, please contact;
Magnus Christensen, CFO, Medivir AB
Telephone: +46 8 5468 3100
E-mail: [email protected]

About fostrox

Fostrox is a type of smart chemotherapy that delivers the cell-killing compound selectively to the tumor while minimizing the harmful effect on normal cells. This is achieved by coupling an active chemotherapy (troxacitabine) with a prodrug tail. The prodrug design enables fostrox to be administered orally and travel directly to the liver where the active substance is released locally in the liver. With this unique mechanism, fostrox has the potential to become the first liver-targeted, orally administered drug that can help patients with various types of liver cancer. A phase 1b monotherapy study with fostrox has been completed and a phase 1b/2a combination study in HCC is ongoing.

About primary liver cancer

Primary liver cancer is the third leading cause of cancer-related deaths worldwide and hepatocellular carcinoma (HCC) is the most common cancer that arises in the liver. Although existing therapies for advanced HCC can extend the lives of patients, treatment benefits are insufficient and death rates remain high. There are approximately 660,000 patients diagnosed with primary liver cancer per year globally and current five-year survival is less than 20 percent2. HCC is a heterogeneous disease with diverse etiologies, and lacks defining mutations observed in many other cancers. This has contributed to the lack of success of molecularly targeted agents in HCC. The limited overall benefit, taken together with the poor overall prognosis for patients with intermediate and advanced HCC, results in a large unmet medical need.

Accent Therapeutics Announces $75 Million Series C Financing to Advance Small Molecule Precision Cancer Therapies

On January 23, 2024 Accent Therapeutics, a biopharmaceutical company pioneering a new class of small molecule precision cancer therapies, reported the completion of a $75 million Series C financing (Press release, Accent Therapeutics, JAN 23, 2024, View Source [SID1234639439]). The financing was led by Mirae Asset Capital Life Science, with participation from other new investors, Mirae Asset Capital, Mirae Asset Venture Investment, Bristol Myers Squibb and Johnson & Johnson Innovation – JJDC, Inc., as well as all existing investors, including The Column Group, Atlas Venture, Droia Ventures, GV, EcoR1 Capital, AbbVie Ventures, The Mark Foundation for Cancer Research, Timefolio Capital (formerly known as NS Investment) and others. In conjunction with the financing, Naveen Krishnan, MD, MPhil, Managing Director of Mirae Asset Capital Life Science will join the Company’s Board of Directors.

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Proceeds from the financing will be used to support the advancement of both lead programs –Accent’s first-in-class DHX9 inhibitor and a potentially best-in-class KIF18A inhibitor – through early clinical development including safety, pharmacokinetics and early efficacy studies.

"We are delighted to announce the backing of an exceptional investor syndicate who share our commitment to advancing innovative therapies for patients with cancer," said Shakti Narayan, PhD, JD, CEO of Accent Therapeutics. "These additional resources position us well to file INDs this year for both our DHX9 and KIF18A programs, and to rapidly progress them through early clinical development."

Accent is developing therapeutics for both novel and known, but suboptimally-addressed, high-impact oncology targets with the potential to benefit large patient populations. The company’s DHX9 inhibitor seeks to address indications with high unmet need, including BRCA loss of function cancers (breast, ovarian), mismatch repair deficient (dMMR) or microsatellite instability-high (MSI-H) cancers (colorectal, endometrial, gastric) and additional undisclosed cancer types. Accent’s second lead program, a KIF18A inhibitor, could also potentially benefit a large patient population across several cancer indications with high unmet need, including ovarian cancer and triple negative breast cancer (TNBC).

"Accent’s focus on targeting cancer cell vulnerabilities in a specific and robust way really stood out as we were evaluating companies for our first investment, " remarked Naveen Krishnan, MD, MPhil, of Mirae Asset Capital Life Science. "They have assembled an incredible team with a successful track record of drug development, and we are excited to partner with the other seasoned investors to support Accent at this pivotal time."

About DHX9
Accent’s lead program is a first-in-class DHX9 inhibitor with the potential to address high unmet need indications not adequately served by existing therapies, including tumors with BRCA loss of function (breast, ovarian), mismatch repair deficient (dMMR) or microsatellite instability-high (MSI-H) cancers (colorectal, endometrial, gastric) and additional undisclosed cancer types representing large patient populations. DHX9 is a DNA/RNA helicase that has been reported to play important roles in replication, transcription, translation, RNA splicing, RNA processing, and maintenance of genomic stability. Hence, this enzyme represents a compelling novel oncology target as inhibition of DHX9 exploits key tumor vulnerabilities, resulting in cancer-specific death. Accent is currently conducting IND-enabling studies evaluating its DHX9 inhibitor.

About KIF18A
Accent’s second lead program is a potential best-in-class inhibitor for KIF18A which may address a large patient population across several cancer indications, including ovarian and triple negative breast cancer (TNBC). KIF18A is a mitotic kinesin motor protein critical for cell division in select tumors with chromosomal instability. A subset of tumor cells with an abnormal number of chromosomes (aneuploid) are sensitive to KIF18A and show rapid cell killing in vitro and in vivo upon KIF18A inhibitor treatment, while cells with normal numbers of chromosomes (euploid) are unaffected. Accent is planning to initiate IND-enabling studies for KIF18A in the first half of 2024.

Caris Life Sciences to Present Research at the 2024 ASCO Genitourinary Cancers Symposium

On January 23, 2024 Caris Life Sciences(Caris), the leading next-generation AI TechBio company and precision medicine pioneer that is actively developing and delivering innovative solutions to revolutionize healthcare and improve the human condition using molecular science and AI, reported that the company and collaborators within the Caris Precision Oncology Alliance (POA) will collectively present eight studies across four tumor types at the 2024 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Genitourinary Cancers Symposium, January 25-27, 2024 in San Francisco (Press release, Caris Life Sciences, JAN 23, 2024, View Source [SID1234639438]). The findings demonstrate the continued and expanded capabilities of Caris’ comprehensive multi-modal database to enable novel insights into cancer that could have profound effects on a patient’s diagnosis, prognosis, care plan and response to treatment.

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"These presentations illustrate how our physicians, scientists and collaborators in the POA are leveraging real-world clinical evidence from over 593,000 lifetime clinical cases, including over 482,000 with matched molecular data and outcomes, in Caris’ unique AI-driven platform to deepen our understanding of cancer and to develop the next breakthrough medicines," said Chadi Nabhan, MD, MBA, FACP, Chairman of the Caris Precision Oncology Alliance. "Caris molecular profiling enables deep exploration of the genetic and immune landscapes of cancer, providing insights into which signaling pathways explain the pathobiology of disease and leading to more precise targeted therapy. That’s a major focus of the wide array of research Caris and our POA collaborators will proudly present at this year’s ASCO (Free ASCO Whitepaper) GU."

Oral Abstract:

A Caris study entitled "Differences in genomic, transcriptomic, and immune landscape of prostate cancer (PCa) based on site of metastasis (mets)" will be presented by Dr. Umang Swami from the Huntsman Cancer Institute on Thursday, January 25 at 4:20 p.m. PST during Rapid Oral Abstract Session A on Prostate Cancer in the Level 3 Ballroom. The research is a collaboration with the Huntsman Cancer Institute at the University of Utah and other POA members.

Compared to primary PCa, both visceral (liver and lung) and non-visceral (lymph node and bone) metastases had higher Androgen Receptor (AR) and interferon g signaling, upregulation of the E2F, G2M checkpoints and MYC target pathways, and were significantly less enriched in macrophage M2, NK, and regulatory T cells. Visceral metastases also had higher neuroendocrine (NEPC) scores and were less enriched for B cells and neutrophils. These data on the molecular and immunologic mechanisms of metastatic tropism in advanced PCa may facilitate future drug development.
Additional Presentations Reveal Potential Impact of Comprehensive Molecular Profiling

Caris will present additional data from studies demonstrating the critical role of comprehensive molecular profiling in the treatment of genitourinary cancers. Poster and abstract summaries highlighting this research will be available onsite at Caris’ booth (#8). The full abstracts will be available through Caris’ website beginning on January 23.

Survival outcomes in patients (pts) with prostatic cancer (PCa) based on pathologically confirmed sites of metastasis (January 25; Poster C7, Abstract 72)
Examination of 6,069 PCa specimens in Caris’ CODEai multi-modal database showed that metastasis to the liver was associated with overall survival significantly shorter than metastasis to the lung, arguing against combining them into the single category of visceral metastases as a stratification factor in randomized clinical trials.

Correlation of PIM kinases with tumor immune microenvironment and clinical presentation of metastatic hormone-sensitive prostate cancer
January 25; Poster J19, Abstract 211)
In a study of 44 patients with treatment-naive metastatic hormone-sensitive prostate cancer (mHSPC), there was a strong association of high expression of PIM kinases with increased MAPK activation score, T cell inflamed score, inflammatory, PSA, AR, MHC class I and MHC class II gene expression, and differential immune cell infiltration. However, this did not significantly translate to a worse clinical presentation of mHSPC. A better understanding of these differences with additional research may provide a rationale for tailored therapeutic approaches for PIM-expressing mHSPC.

The influence of the germline HSD3B1 adrenal-permissive variant (c.1100 C) on somatic alteration landscape, transcriptome, and immune-cell infiltration in prostate cancer (January 25; Poster K3, Abstract 215)
In a study of 5,421 prostate cancer biopsies from the Caris Life Sciences database, the homozygous adrenal-permissive HSD3B1 variant (c.1100 CC) was characterized by elevated AR signaling and MAPK activation and a unique immune-cell regulatory landscape, with higher B7-H3 expression, increased intratumoral dendritic cells and decreased immunosuppressive neutrophils, suggesting that B7-H3–targeted therapies might be effective against this class of cancer.

The opposing effects of Class 1B and Class 2 FOXA1 mutations in prostate cancer (January 25; Poster K4, Abstract 216)
Alterations in the FOXA1 transcription factor are present in 16% of prostate cancers (PCa), but different alterations exhibit divergent molecular and clinical profiles. In a study of more than 4,000 primary and metastatic PCa samples, missense mutations in the Wing2 region of FOXA1 (a.a. 248-269) had better response to androgen deprivation therapy (ADT), whereas mutations in a.a. R219, a highly conserved DNA contact residue, were associated with a neuroendocrine phenotype and showed poor survival with ADT.

Canonical Wnt signaling pathway (WSP) alterations in metastatic prostate cancer (January 25; Poster K9, Abstract 221)
In a study of 4,150 total PCa samples, 722 with aberrant canonical Wnt signaling (WSP-act), WSP-act tumors had pronounced upregulation of ROR1 gene expression and augmented levels of M2 macrophages, suggesting that ROR1 may contribute to immune evasion in WSP-act mPCa.

Comprehensive analysis of targetable alterations in urachal cancer by NGS
(January 26; Poster K7, Abstract 663)
In a comprehensive characterization the molecular and immune landscape of urachal cancer (UrC), UrC tumors rarely harbored predictive markers of response to immunotherapy, suggesting limited efficacy in this patient population. However, the recurrence of MAPK alterations and associated pathway activation in UrC warrants further investigation of MAPK-targeted therapies in prospective clinical trials.

IL-6 and PIM1 expression in renal cell carcinoma
(January 27; Poster K11, Abstract 470)
Based on the hypothesis that an IL-6/JAK/STAT pathway regulates the expression of PIM1 in renal cell carcinoma (RCC) as in pancreatic and breast cancer, the transcriptomes of RCC samples in the Caris multi-modal database were analyzed, showing that PIM1 expression was significantly increased in metastatic relative to primary RCC. IL-6 expression was up to 6.5-fold higher in RCC patients with PIM1 overexpression. Outcomes data showed that PIM1 overexpression was associated with decreased overall survival for RCC patients independent of treatment received. Since multiple FDA-approved agents are available that target this pathway, further investigation is warranted to determine the efficacy of these agents in pre-clinical models and clinical trials of RCC.
The POA includes 90 cancer centers, academic institutions, research consortia and healthcare systems, including 42 NCI-designated cancer centers, collaborating to advance precision oncology and biomarker-driven research. POA members work together to establish and optimize standards of care for molecular testing through innovative research focused on predictive and prognostic markers that improve the clinical outcomes for cancer patients.

Akeso Presented Promising Results of Cadonilimab and Lenvatinib in Combination with TACE in uHCC at 2024 ASCO GI

On January 23, 2024 Akeso, Inc. (9926.HK) ("Akeso," "we," or the "Company") reported that the Company presented the promising phase II results of cadonilimab (a tetravalent PD-1/CTLA-4 bispecific antibody) and Lenvatinib (Len) combined with TACE for the treatment of mid- and advanced-stage hepatocellular carcinoma (HCC) in a poster at the 2024 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Gastrointestinal Cancers Symposium in San Francisco, California (Press release, Akeso Biopharma, JAN 23, 2024, View Source [SID1234639437]). Based on the encouraging results, the company plans to further explore this combination therapy for the mid- and advanced-stage HCC indication.

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AK104-216 is an open-label, multicenter phase II trial (NCT05319431). As of August 15, 2023, 60 patients received at least once Cadonilimab and the median duration of follow-up was 5.1 months. Cadonilimab and Lenvatinib combined with TACE showed great tumor response: The ORR and DCR were 85.0% and 95% per mRECIST. 15% subjects achieved CR and 70% subjects achieved PR. The median PFS was not reached, 6-month PFS rate and 9-month PFS rate was 75.6% and 60.4%, respectively. Cadonilimab and Lenvatinib combined with TACE showed manageable safety in mid- and advanced-stage HCC.

HCC typically has an insidious onset, with over 80% of patients being diagnosed in the middle to late stages of the disease. The low rate of radical resection and poor overall prognosis further compound the challenges associated with HCC. Transarterial chemoembolization (TACE) is a standard therapy recommended for intermediate-stage unresectable hepatocellular carcinoma (uHCC) but has unsatisfying tumor control due to the increasing risk of tumor angiogenesis. Immune-checkpiont inhibitors, in combination with targeted therapy and local therapy, have been developed as promising treatment for mid- and advanced-stage HCC.

Cadonilimab and Lenvatinib combined with TACE have demonstrated promising efficacy and manageable toxicity in treating mid- and advanced-stage HCC. Patients can expect to benefit from tumor progression control after TACE and lasting survival. Akeso is actively preparing a clinical study of this therapy in mid- and advanced-stage HCC, which will be registrational. Furthermore, Akeso is accelerating the progress of the registrational Phase III clinical study of cadonilimab monotherapy for postoperative adjuvant treatment of hepatocellular carcinoma. The enrollment for this study is expected to be completed in 2024.

Taiho Oncology Announces Publication of Final Results of the Phase 3 ASCERTAIN Clinical Trial of Oral Decitabine and Cedazuridine Fixed Dose Combination (INQOVI®) in Patients With MDS and CMML

On January 23, 2024 Taiho Oncology, Inc. reported publication of the final results from the pivotal ASCERTAIN clinical trial of fixed-dose oral decitabine and cedazuridine (INQOVI) compared to intravenous decitabine in adults with intermediate and high-risk myelodysplastic syndromes (MDS) including chronic myelomonocytic leukemia (CMML) (Press release, Taiho, JAN 23, 2024, View Source [SID1234639436]).

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The ASCERTAIN trial was the first Phase 3 trial to demonstrate pharmacologic equivalence between an oral and an intravenous (IV) formulation of a hypomethylating agent for use in the treatment of patients with MDS or CMML. As reported in the January 2 issue of The Lancet Haematology, median overall survival (mOS) in the trial population was approximately 32 months.1 In addition, the overall response rate was 62% in the intent to treat patient population. The percentage of patients in this trial who moved to transplantation reached 20%, exceeding expected transplantation rates in patients receiving hypomethylating agents for MDS and CMML.1

Safety findings from the study were comparable with those previously observed with IV decitabine. The most common treatment-emergent adverse events of thrombocytopenia, neutropenia and anemia were consistent with expected adverse events with parenteral hypomethylating agent treatment.

The data from the study supported the simultaneous approval of INQOVI by the U.S. Food and Drug Administration and Health Canada in July 2020 for the treatment of adult patients with myelodysplastic syndromes (MDS), including previously treated and untreated, de novo and secondary MDS with the following French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, and chronic myelomonocytic leukemia [CMML]) and intermediate-1, intermediate-2, and high-risk International Prognostic Scoring System groups.2

"Until recently, azacitidine and decitabine, both widely used hypomethylating agents, were available only in parenteral form, requiring patients with MDS and CMML to travel to treatment centers daily for 5 or 7 consecutive days of each 28-day treatment cycle," said Guillermo Garcia-Manero, MD, Professor, Department of Leukemia, Division of Cancer Medicine, the University of Texas MD Anderson Cancer Center, Houston, and the lead author on the publication. "The ASCERTAIN study has demonstrated that the orally delivered fixed dose combination of decitabine and cedazuridine is an alternative option to parenteral administration of decitabine for patients with these diseases. The observed median overall survival of greater than 30 months in the ASCERTAIN study compared with historical controls is encouraging."

Added Tehseen Salimi, MD, MHA, Senior Vice President and Head of Medical Affairs, Taiho Oncology, Inc., "Patients living with MDS and CMML can benefit from the convenience of an at-home hypomethylating agent treatment that may potentially reduce the number of office visits and the travel that comes with it."

About the ASCERTAIN Trial
The Phase 3 ASCERTAIN clinical trial was a multicenter, randomized, open-label, crossover pharmacokinetics (PK) study comparing oral decitabine (35mg) and cedazuridine (100mg) fixed-dose combination tablet given once daily for 5 days on a 28-day cycle to IV decitabine (20mg/m2) administered as a daily 1-hour IV infusion for 5 days on a 28-day cycle, in the first 2 cycles in patients with MDS and CMML. Patients continued to receive oral decitabine and cedazuridine from Cycle 3 onwards. The primary endpoint of the study was total 5-day area-under-the-curve (AUC) equivalence of oral decitabine and cedazuridine and IV decitabine.

For more information about ASCERTAIN, please visit: View Source;draw=3&rank=19.

INDICATIONS
Decitabine and cedazuridine, marketed under the brand name INQOVI, is indicated for treatment of adult patients with myelodysplastic syndromes (MDS), including previously treated and untreated, de novo and secondary MDS with the following French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, and chronic myelomonocytic leukemia [CMML]) and intermediate-1, intermediate-2, and high-risk International Prognostic Scoring System groups.2

INQOVI is the first and only oral hypomethylating agent approved by the FDA and by Health Canada for the treatment of adults with intermediate and high-risk MDS including CMML.

Commercialization of INQOVI in the U.S. and Canada is conducted by Taiho Oncology, Inc. and Taiho Pharma Canada, Inc., respectively.

IMPORTANT SAFETY INFORMATION WARNINGS AND PRECAUTIONS

Myelosuppression
Fatal and serious myelosuppression can occur with INQOVI. Based on laboratory values, new or worsening thrombocytopenia occurred in 82% of patients, with Grade 3 or 4 occurring in 76%. Neutropenia occurred in 73% of patients, with Grade 3 or 4 occurring in 71%. Anemia occurred in 71% of patients, with Grade 3 or 4 occurring in 55%. Febrile neutropenia occurred in 33% of patients, with Grade 3 or 4 occurring in 32%. Myelosuppression (thrombocytopenia, neutropenia, anemia, and febrile neutropenia) is the most frequent cause of INQOVI dose reduction or interruption, occurring in 36% of patients. Permanent discontinuation due to myelosuppression (febrile neutropenia) occurred in 1% of patients. Myelosuppression and worsening neutropenia may occur more frequently in the first or second treatment cycles and may not necessarily indicate progression of underlying MDS.

Fatal and serious infectious complications can occur with INQOVI. Pneumonia occurred in 21% of patients, with Grade 3 or 4 occurring in 15%. Sepsis occurred in 14% of patients, with Grade 3 or 4 occurring in 11%. Fatal pneumonia occurred in 1% of patients, fatal sepsis in 1%, and fatal septic shock in 1%.

Obtain complete blood cell counts prior to initiation of INQOVI, prior to each cycle, and as clinically indicated to monitor response and toxicity. Administer growth factors and anti‑infective therapies for treatment or prophylaxis as appropriate. Delay the next cycle and resume at the same or reduced dose as recommended.

Embryo-Fetal Toxicity
INQOVI can cause fetal harm. Advise pregnant women of the potential risk to a fetus. Advise patients to use effective contraception during treatment and for 6 months (females) or 3 months (males) after last dose.

ADVERSE REACTIONS
Serious adverse reactions in > 5% of patients included febrile neutropenia (30%), pneumonia (14%), and sepsis (13%). Fatal adverse reactions included sepsis (1%), septic shock (1%), pneumonia (1%), respiratory failure (1%), and one case each of cerebral hemorrhage and sudden death.

The most common adverse reactions (≥ 20%) were fatigue (55%), constipation (44%), hemorrhage (43%), myalgia (42%), mucositis (41%), arthralgia (40%), nausea (40%), dyspnea (38%), diarrhea (37%), rash (33%), dizziness (33%), febrile neutropenia (33%), edema (30%), headache (30%), cough (28%), decreased appetite (24%), upper respiratory tract infection (23%), pneumonia (21%), and transaminase increased (21%). The most common Grade 3 or 4 laboratory abnormalities (≥ 50%) were leukocytes decreased (81%), platelet count decreased (76%), neutrophil count decreased (71%), and hemoglobin decreased (55%).

USE IN SPECIFIC POPULATIONS

Lactation
Because of the potential for serious adverse reactions in the breastfed child, advise women not to breastfeed during treatment with INQOVI and for 2 weeks after the last dose.

Renal Impairment
No dosage modification of INQOVI is recommended for patients with mild or moderate renal impairment (creatinine clearance [CLcr] of 30 to 89 mL/min based on Cockcroft-Gault). Due to the potential for increased adverse reactions, monitor patients with moderate renal impairment (CLcr 30 to 59 mL/min) frequently for adverse reactions. INQOVI has not been studied in patients with severe renal impairment (CLcr 15 to 29 mL/min) or end-stage renal disease (ESRD: CLcr <15 mL/min).

Please see the accompanying Full Prescribing Information.

About Myelodysplastic Syndromes (MDS) and Chronic Myelomonocytic Leukemia (CMML)
Myelodysplastic syndromes are a heterogeneous group of hematopoietic stem cell disorders characterized by dysplastic changes in myeloid, erythroid, and megakaryocytic progenitor cells, and associated with cytopenias affecting one or more of the three lineages. U.S. incidence of MDS is estimated to be 10,000 cases per year, although the condition is thought to be under-diagnosed.3,4 The prevalence has been estimated to be from 60,000 to 170,000 in the U.S.5 MDS may evolve into acute myeloid leukemia (AML) in one-third of patients.6 The prognosis for MDS patients is poor; patients die from complications associated with cytopenias (infections and bleeding) or from transformation to AML.

CMML is a clonal hematopoietic malignancy characterized by accumulation of abnormal monocytes in the bone marrow and in blood. The incidence of CMML in the U.S. is approximately 1,100 new cases per year,7 and CMML may transform into AML in 15% to 30% of patients.8

About Decitabine and Cedazuridine Fixed-Dose Combination
This product is an orally administered, fixed dose combination of the approved anti-cancer DNA hypomethylating agent, decitabine, together with cedazuridine,3 an inhibitor of cytidine deaminase.4 By inhibiting cytidine deaminase in the gut and the liver, the fixed dose combination is designed to allow for oral delivery of decitabine over five days in a given cycle to achieve comparable systemic exposure to IV decitabine administered over five days.

The oral decitabine and cedazuridine fixed-dose combination has been evaluated in a Phase 1/2 pharmacokinetics-guided dose escalation and dose confirmation study, and a Phase 3 exposure equivalence study in patients with MDS and CMML – the ASCERTAIN study.