CDKN2B

BERKELEY HEIGHTS, N.J., March 07, 2024 (GLOBE NEWSWIRE) -- Cyclacel Pharmaceuticals Inc. (NASDAQ: CYCC, NASDAQ: CYCCP; "Cyclacel" or the "Company"), a biopharmaceutical company developing innovative medicines based on cancer cell biology, today announced that preclinical proof-of-concept data with the Company’s fadraciclib will be presented at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2024, being held April 5-10 in San Diego, California. The data will be presented at three poster sessions and report activity and antitumor effects of fadraciclib in biliary tract cancer, lung cancer, Richter transformation and lymphoma cell lines. Details of the presentations are as follows: Title: The CDK2/9 inhibitor fadraciclib is active in Richter transformation and lymphoma cell lines by targeting both cell survival and proliferation Abstract No: 518 / 15 Session Topic: Session PO.ET05.01 - Cell Cycle, Transcription Regulation, and Anticancer Drug Action Date and Time: April 7, 2024, 1:30 PM - 5:00 PM PT Location: Exhibition Hall, Section 21 Title: Elucidation of the fates of CDK2 inhibited aneuploid and residual lung cancers Abstract No: 2117 / 8 Session Topic: Session PO.ET07.02 - Pharmacodynamic Biomarkers of Drug Response Date and Time: April 8, 2024, 9:00 AM - 12:30 PM PT Location: Exhibition Hall, Section 30 Title: Anti-tumor effects of fadraciclib, CDK2/9 inhibitor, in biliary tract cancer Abstract No: 5711 / 11 Session Topic: Session PO.MCB01.01 - Pharmacologic Targeting of Cell Cycle Proteins Date and Time: April 9, 2024, 1:30 PM - 5:00 PM PT Location: Exhibition Hall, Section 18 About Cyclin-Dependent Kinases and Fadraciclib Cyclin-dependent kinases (CDKs) are critical for cell cycle control and transcriptional regulation. Dysregulated CDKs have been linked to the cancer hallmarks of uncontrolled proliferation and increased cancer cell survival. Fadraciclib is a highly selective, potent, orally and intravenously available, next generation inhibitor of CDK2 and CDK9. By inhibiting CDK2 and CDK9 fadraciclib causes apoptotic death through anaphase catastrophe of cancer cells at sub-micromolar concentrations. To date single agent activity, including CR, PR and SD, has been observed in patients with advanced endometrial, squamous NSCLC lung cancer and T-cell lymphoma. Encouraging signals of activity were observed in patients with advanced cervical, hepatocellular, ovarian and pancreatic cancers. 065-101 Study of Oral Fadraciclib Oral fadraciclib is being tested in a Phase 1/2 trial for the treatment of advanced solid tumors and lymphoma (065-101; NCT#04983810). A total of 29 patients have been treated as monotherapy in this ongoing study. The study is enrolling unselected, all comer patients with advanced solid tumors and lymphoma. The Phase 2 part of the 065-101 study is designed to further evaluate fadra safety and efficacy in up to 8 cohorts defined by histology and/or NGS. The study is powered to demonstrate response in the molecular subtype suggested by the Phase 1 data and others that may be sensitive. CDKN2A, CDKN2B, MTAP deletions CDKN2A gene deletions occur in over 40% of several solid tumors, including glioma, head and neck, pancreatic, esophageal, lung (incl. squamous), bladder, melanoma, and others. CDKN2B deletions occur in over 30% of several solid tumors, including bladder, glioma, pancreatic, esophageal, lung (incl. squamous), head and neck, melanoma, and others. MTAP deletions occur in over 25% of several solid tumors, including glioma, mesothelioma, pancreatic, bladder, esophageal and others. MTAP deletion confers dependency on the PRMT5 enzyme in cancer cells which was identified as a synthetic lethal target for MTAP deleted cancers. About Cyclacel Pharmaceuticals, Inc. Cyclacel is a clinical-stage, biopharmaceutical company developing innovative cancer medicines based on cell cycle, transcriptional regulation and mitosis biology. The transcriptional regulation program is evaluating fadraciclib, a CDK2/9 inhibitor, and the anti-mitotic program CYC140, a PLK1 inhibitor, in patients with both solid tumors and hematological malignancies. Cyclacel's strategy is to build a diversified biopharmaceutical business based on a pipeline of novel drug candidates addressing oncology and hematology indications. For additional information, please visit . Forward-looking Statements This news release contains certain forward-looking statements that involve risks and uncertainties that could cause actual results to be materially different from historical results or from any future results expressed or implied by such forward-looking statements. Such forward-looking statements include statements regarding, among other things, the efficacy, safety and intended utilization of Cyclacel’s product candidates, the conduct and results of future clinical trials, plans regarding regulatory filings, future research and clinical trials and plans regarding partnering activities. Factors that may cause actual results to differ materially include the risk that product candidates that appeared promising in early research and clinical trials do not demonstrate safety and/or efficacy in larger-scale or later clinical trials, trials may have difficulty enrolling, Cyclacel may not obtain approval to market its product candidates, the risks associated with reliance on outside financing to meet capital requirements, the potential effects of the COVID-19 pandemic, and the risks associated with reliance on collaborative partners for further clinical trials, development and commercialization of product candidates. You are urged to consider statements that include the words "may," "will," "would," "could," "should," "believes," "estimates," "projects," "potential," "expects," "plans," "anticipates," "intends," "continues," "forecast," "designed," "goal," or the negative of those words or other comparable words to be uncertain and forward-looking. For a further list and description of the risks and uncertainties the Company faces, please refer to our most recent Annual Report on Form 10-K and other periodic and other filings we the Securities and Exchange Commission and are available at . Such forward-looking statements are current only as of the date they are made, and we assume no obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise. Contacts Company: Paul McBarron, (908) 517-7330, pmcbarron@cyclacel.com Investor Relations: Grace Kim, IR@cyclacel.com © Copyright 2024 Cyclacel Pharmaceuticals, Inc. All Rights Reserved. The Cyclacel logo and Cyclacel® are trademarks of Cyclacel Pharmaceuticals, Inc.

- Patient Pharmacodynamic Data Show Decrease in CDKN2A, CDKN2B, and PRMT5 Protein Levels - - A Squamous Non-Small Cell Lung Cancer Patient with CDKN2B Deletion Achieved Marked Tumor Shrinkage after One Cycle - - Retrospective Analysis Identified CDKN2A, CDKN2B and/or MTAP Deletions in Four Patients Previously Dosed with Fadra Achieving Responses or Stable Disease - - Forthcoming Phase 2 Study to Further Evaluate Fadra Efficacy - BERKELEY HEIGHTS, N.J., Dec. 18, 2023 (GLOBE NEWSWIRE) -- Cyclacel Pharmaceuticals, Inc. (NASDAQ: CYCC, NASDAQ: CYCCP; "Cyclacel" or the "Company"), a biopharmaceutical company developing innovative medicines based on cancer cell biology, announced today interim results from its Phase 1, dose escalation 065-101 study of fadraciclib (“fadra”) in patients with advanced solid tumors and lymphoma. “As we approach the end of the year we are excited to report that fadra continues to demonstrate anticancer activity as a single agent based on interim data reviewed to date from our 065-101 study,” said Spiro Rombotis, President and Chief Executive Officer. “The data suggest tumor sensitivity in patients with one or more of three abnormalities, CDKN2A, CDKN2B and/or MTAP deletion subject to confirmation in further studies. We believe there is great unmet medical need and industry interest in the cancer patient populations identified by these abnormalities, which are closely located on chromosome 9 and are often co-deleted. The Phase 2 part of 065-101 is designed to evaluate fadra safety and efficacy in cohorts defined by histology and/or next generation sequencing (NGS). In addition, our plogosertib dose escalation study is progressing well. Based on interim data reviewed to date, good tolerability and anticancer activity of plogosertib as a single agent have been observed in multiple patients with various solid tumors.” “We are excited to see shrinkage of 22% in the sum of all target lesions after one cycle of fadra monotherapy in a squamous non-small cell lung cancer (NSCLC) patient with CDKN2B deletion refractory to standard of care chemotherapy and immunotherapy,” said Mark Kirschbaum, M.D., Chief Medical Officer. “After retrospectively analyzing a subset of previously treated Phase 1 patients who experienced clinical benefit with fadra, we found four patients with CDKN2A, CDKN2B and/or MTAP deletions. These included an endometrial cancer patient who achieved CR and over three years of treatment in a previous study of fadra monotherapy and was found to have all three abnormalities. Further, pharmacodynamic data from patient biospecimens at dose levels 5 and 6A suggest that CDKN2A, CDKN2B, and PRMT5 protein levels are transiently decreased over the 4 to 8 hour half-life of the fadra dose, which we believe makes the tumor sensitive to CDK2 inhibition by fadra. Although these hypothesis-generating data are limited and cannot be generalized, we believe that patients with these types of tumors should be evaluated in the ongoing and subsequent studies.” 065-101 Study of Oral FadraciclibIn the ongoing 065-101 study of oral fadra, a CDK2/9 inhibitor, a total of 29 patients have been treated as monotherapy. The study is enrolling unselected, all comer patients with advanced solid tumors and lymphoma. Six patients have been treated on dose level 6A (125mg twice daily for 5 days per week, 4 out of 4 weeks). The sixth patient on dose level 6A with pancreatic cancer and CDKN2A deletion enrolled on the study experienced dose-limiting toxicity (DLT) of hyperglycemia. The patient, who has a diabetic profile history and was on metformin treatment, remains on study as blood glucose level was managed. A previous patient on dose level 6A with a pre-diabetic profile had DLT of hyperglycemia which also resolved rapidly. The previous dose level 5 (100mg twice daily for 5 days per week, 4 out of 4 weeks) on this schedule accrued six patients with no DLT and per protocol is safe for continued development. Dose level 6B (150mg once daily for 7 days per week, 4 out of 4 weeks) continues accrual with two patients treated, which are ongoing at three and five cycles of treatment. To date single agent activity, including CR, PR and SD, has been observed in patients with advanced endometrial, squamous NSCLC lung cancer and T-cell lymphoma. Encouraging signals of activity were observed in patients with advanced cervical, hepatocellular, ovarian and pancreatic cancers. The Company believes that fadra’s inhibition of CDK2 and CDK9 may be superior to inhibiting either CDK2 or CDK9 alone. Fadra tablets can be given orally with repeat dosing which has led to transient suppression of anti-apoptosis proteins with generally good tolerability and no Grade 3 or higher hematological toxicity in the first cycle. The Phase 2 part of the 065-101 study is designed to further evaluate fadra safety and efficacy in up to 8 cohorts defined by histology and/or NGS. The study is powered to demonstrate response in the molecular subtype suggested by the Phase 1 data and others that may be sensitive. CDKN2A, CDKN2B, MTAP deletionsCDKN2A gene deletions occur in over 40% of several solid tumors, including glioma, head and neck, pancreatic, esophageal, lung (incl. squamous), bladder, melanoma, and others. CDKN2B deletions occur in over 30% of several solid tumors, including bladder, glioma, pancreatic, esophageal, lung (incl. squamous), head and neck, melanoma, and others. MTAP deletions occur in over 25% of several solid tumors, including glioma, mesothelioma, pancreatic, bladder, esophageal and others.1 MTAP deletion confers dependency on the PRMT5 enzyme in cancer cells which was identified as a synthetic lethal target for MTAP deleted cancers. 140-101 Phase 1 Study of Oral PlogosertibIn the 140-101 study of oral plogosertib, PLK1 inhibitor, as monotherapy, patients are being recruited at dose level 5. The anticancer activity observed at low levels of continuous exposure may be due to plogosertib’s novel epigenetic mechanism. To date, 15 patients have been recruited at five dose escalation levels. Encouraging signals of activity were observed in five patients with advanced biliary, ovarian, NSCLC and other cancers. The Company expects to announce details of plogosertib’s differentiated, epigenetic mechanism and biomarkers which may identify patients with sensitive tumors, after preclinical studies at collaborating laboratories are completed. About Cyclacel Pharmaceuticals, Inc. Cyclacel is a clinical-stage, biopharmaceutical company developing innovative cancer medicines based on cell cycle, transcriptional regulation, epigenetics and mitosis biology. The transcriptional regulation program is evaluating fadraciclib, a CDK2/9 inhibitor, and the epigenetic/anti-mitotic program plogosertib, a PLK1 inhibitor, in patients with both solid tumors and hematological malignancies. Cyclacel's strategy is to build a diversified biopharmaceutical business based on a pipeline of novel drug candidates addressing oncology and hematology indications. For additional information, please visit www.cyclacel.com. Forward-looking StatementsThis news release contains certain forward-looking statements that involve risks and uncertainties that could cause actual results to be materially different from historical results or from any future results expressed or implied by such forward-looking statements. Such forward-looking statements include statements regarding, among other things, the efficacy, safety and intended utilization of Cyclacel’s product candidates, the conduct and results of future clinical trials, plans regarding regulatory filings, future research and clinical trials and plans regarding partnering activities. Factors that may cause actual results to differ materially include, without limitation: interim results of a clinical trial are not necessarily indicative of final results and one or more of the clinical outcomes may materially change as patient enrollment continues, following more comprehensive reviews of the data and as more patient data becomes available, including the risk that unconfirmed responses may not ultimately result in confirmed responses to treatment after follow-up evaluations; the risk that product candidates that appeared promising in early research and clinical trials do not demonstrate safety and/or efficacy in larger-scale or later clinical trials; potential delays in the commencement, enrollment and completion of clinical trials; Cyclacel may not obtain approval to market its product candidates; the risks associated with reliance on outside financing to meet capital requirements; the potential effects of the COVID-19 pandemic; and the risks associated with reliance on collaborative partners for further clinical trials, development and commercialization of product candidates. You are urged to consider statements that include the words "may," "will," "would," "could," "should," "believes," "estimates," "projects," "potential," "expects," "plans," "anticipates," "intends," "continues," "forecast," "designed," "goal," or the negative of those words or other comparable words to be uncertain and forward-looking. For a further list and description of the risks and uncertainties the Company faces, please refer to our most recent Annual Report on Form 10-K, as amended, and other periodic and other filings we file with the Securities and Exchange Commission and are available at www.sec.gov. Such forward-looking statements are current only as of the date they are made, and we assume no obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise. Contacts Company:Paul McBarron, (908) 517-7330, pmcbarron@cyclacel.comInvestor Relations:Grace Kim, IR@cyclacel.com © Copyright 2023 Cyclacel Pharmaceuticals, Inc. All Rights Reserved. The Cyclacel logo and Cyclacel® are trademarks of Cyclacel Pharmaceuticals, Inc. SOURCE: Cyclacel Pharmaceuticals, Inc. _______________ 1 www.cbioportal.org.

Treatment with futibatinib resulted in durable responses and survival surpassing historical data with chemotherapy in patients with previously treated disease. Patients in the study reported stable quality of life over nine months of treatment. Data supported U.S. Food and Drug Administration accelerated approval of LYTGOBI® (futibatinib) tablets in September 2022; continued approval may be contingent upon a confirmatory trial(s). PRINCETON, N.J., Jan. 18, 2023 /PRNewswire/ -- Taiho Oncology, Inc. today announced the publication of results from the pivotal Phase 2 FOENIX*-CCA2 clinical trial of futibatinib in the January 19, 2023 issue of The New England Journal of Medicine (NEJM). The article, "Futibatinib for Intrahepatic Cholangiocarcinoma with FGFR2 Fusions/Rearrangements," reports on data from the FOENIX-CCA2 trial, a global open-label study evaluating patients with previously treated, unresectable, locally advanced or metastatic intrahepatic cholangiocarcinoma (iCCA) harboring fibroblast growth factor receptor 2 (FGFR2) gene fusions or other rearrangements. These data supported the U.S. Food and Drug Administration (FDA) accelerated approval of futibatinib tablets – brand name LYTGOBI® – in September 2022 for the treatment of adult patients with previously treated, unresectable, locally advanced or metastatic iCCA harboring FGFR2 gene fusions or other rearrangements. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).1 In the FOENIX-CCA2 trial, futibatinib showed clinically meaningful benefit in previously treated patients with FGFR2 fusion/rearrangement-positive iCCA, including an objective response rate of 42%, as assessed by independent review, and a median response duration of 9.7 months. Treatment with futibatinib resulted in durable responses and survival that surpassed historical data with chemotherapy in patients with previously treated iCCA. According to the investigators, these data suggest that a molecularly-targeted agent like futibatinib can substantially improve outcomes for patients with iCCA harboring FGFR2 fusions/rearrangements. "The FOENIX-CCA2 trial results demonstrate that futibatinib is an effective treatment for FGFR2 fusion/rearrangement positive cholangiocarcinoma. Its activity and safety profile offer a new treatment in this setting. These data reinforce the importance of molecular profiling in cholangiocarcinoma and represent a step forward for patients facing a difficult disease," said Lipika Goyal, MD, MPhil, the lead investigator for FOENIX-CCA2 and previously a medical oncologist at Mass General Cancer Center and now Associate Professor and Director of Gastrointestinal Cancer at the Stanford School of Medicine. Cholangiocarcinoma is an aggressive cancer of the bile ducts and is diagnosed in approximately 8,000 individuals each year in the U.S.2 This includes both intrahepatic (inside the liver) and extrahepatic (outside the liver) forms of the disease. Approximately 10-16% of patients with iCCA have FGFR2 gene rearrangements, including fusions, which promote tumor proliferation.3,4,5,6,7 Historically, patients with iCCA have a five-year overall survival rate of less than 8% with a median overall survival of approximately one year in advanced stages,8,9 underscoring the unmet need for additional second-line therapies. Futibatinib is an oral, potent, selective small-molecule inhibitor of FGFR1, 2, 3 and 4.1 It covalently binds to FGFR and inhibits the signaling pathway,1 a unique mode of binding compared to the other currently approved FGFR inhibitors, which are reversible ATP-competitive inhibitors.10,11,12 Key Findings From the FOENIX-CCA2 Trial Among the 103 patients enrolled in the study, futibatinib showed a confirmed objective response rate of 42% (95% confidence interval [CI], 32%-52%), according to Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1, as the primary endpoint of the study. Patients responding to futibatinib had a median duration of response, a key secondary endpoint, of 9.7 months (95% CI, 7.6-17.0). The disease control rate was 83% (95% CI, 74%-89%). At data cutoff for the primary analysis on October 1, 2020, median follow-up was 17.1 months (range, 10.1-29.6) and median treatment duration was 9.1 months. Objective responses were observed across all protocol-specified subgroups, including in patients aged at least 65 years and those with one, two or three or more prior treatment lines. Median progression-free survival was 9.0 months (95% CI, 6.9-13.1) and median overall survival was 21.7 months (95% CI, 14.5 to not reached). Similar response and survival data were documented at extended follow-up, 8.0 months after the primary analysis. Patient-reported outcomes were evaluated as a prespecified secondary objective and results showed stable quality of life over 9.0 months for trial participants. Throughout the observed time period, there were no meaningful changes from baseline across the observed study period in any of the EORTC-QLQ-c30 quality of life (QoL) scales, including physical, role, cognitive, emotional or social domains. In addition, the EQ-5D Visual Analog Scale did not reveal any significant changes in perceived health status across the observed study period. All patients experienced at least one adverse event of any cause. The most common (≥25%) treatment-related adverse reactions were hyperphosphatemia (85%), alopecia (33%), dry mouth (30%), diarrhea (28%), dry skin (27%) and fatigue (25%). Treatment-related adverse events led to treatment discontinuation in 2% of patients, and no new safety concerns were reported with extended follow-up. No treatment-related deaths occurred. Genomic Profiling Analysis to Identify FGFR2 Rearrangements The tumor molecular-profile analysis indicated that responses did not correlate with FGFR2 fusion-partner status or co-occurring alterations in tumor suppressor or oncogenes. Response rates were 42% and 45% in patients with BICC1- and non-BICC1 fusions, respectively, and ORR ranged from 35% to 49% in patients with or without BAP1, TP53, CDKN2A or CDKN2B co-alterations. Of note, response rates and PFS were similar in patients with and without TP53 co-alterations. As FGFR2 fusions and other rearrangements are an important actionable alteration in cholangiocarcinoma, utilizing a practical, high-performance method for identifying this therapeutic target will contribute to improved care of patients with this disease. Accurate tumor profiling to identify individuals with FGFR2 gene rearrangements can be challenging if tissue from tumor biopsy is limited. In addition, the failure rate of tissue biopsy profiling in metastatic CCA is as high as 26.8%.13 Circulating tumor DNA (ctDNA) profiling offers a non-invasive alternative for patients with no tumor tissue available or failed attempts at tissue profiling. Although the FGFR2 fusion/rearrangement detection rate from blood samples by ctDNA assays has historically been low with some platforms,14 the fusion partner-agnostic ctDNA platform utilized in the correlative analyses in the FOENIX-CCA2 trial identified FGFR2 fusions or rearrangements in 87% of patients evaluated.15 Impact on Treatment Guidelines for Biliary Tract Cancers In October 2022, futibatinib was included in the latest National Comprehensive Cancer Network® Clinical Practice Guidelines (NCCN Guidelines®) in Oncology for Hepatobiliary Cancers as a subsequent-line therapy for biliary tract cancers if disease progression occurs. Futibatinib is listed as Category 2A, useful in certain circumstances for CCA with FGFR2 fusions or rearrangements. In addition, the latest European Society for Medical Oncology (ESMO) Clinical Practice Guideline for diagnosis, treatment and follow-up of biliary tract cancer include that, where available, FGFR inhibitors, including futibatinib, are recommended for the treatment of patients with FGFR2 fusions whose disease has progressed after ≥1 prior line of systemic therapy. Futibatinib was discovered by Taiho Oncology's parent company, Taiho Pharmaceutical Co., Ltd., which continues to co-develop this product for other potential tumor types. About LYTGOBI INDICATION AND USAGE LYTGOBI is indicated for the treatment of adult patients with previously treated, unresectable, locally advanced or metastatic intrahepatic cholangiocarcinoma harboring fibroblast growth factor receptor 2 (FGFR2) gene fusions or other rearrangements. This indication is approved under accelerated approval based on overall response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s). IMPORTANT SAFETY INFORMATION WARNINGS AND PRECAUTIONS Ocular Toxicity: Retinal Pigment Epithelial Detachment (RPED), which may cause symptoms such as blurred vision, occurred in 9% of 318 patients who received LYTGOBI across clinical trials. The median time to first onset of RPED was 40 days. Perform a comprehensive ophthalmological examination, including optical coherence tomography (OCT) of the macula, prior to initiation of therapy, every 2 months for the first 6 months, and every 3 months thereafter. For onset of visual symptoms, refer patients for ophthalmologic evaluation urgently, with follow-up every 3 weeks until resolution or discontinuation of LYTGOBI. Withhold or reduce the dose of LYTGOBI as recommended. Dry Eye/Corneal Keratitis: Among 318 patients who received LYTGOBI across clinical trials, dry eye occurred in 15% of patients. Treat patients with ocular demulcents as needed. Hyperphosphatemia and Soft Tissue Mineralization: Hyperphosphatemia, which can cause soft tissue mineralization, calcinosis, nonuremic calciphylaxis, and vascular calcification was reported in 88% of 318 patients treated with LYTGOBI across clinical trials with a median time of onset of 5 days (range 3-117). Phosphate binders were received by 77% of patients who received LYTGOBI. Monitor for hyperphosphatemia throughout treatment. Initiate a low-phosphate diet and phosphate-lowering therapy when serum phosphate level is ≥5.5 mg/dL; initiate or intensify phosphate-lowering therapy when >7 mg/dL; reduce dose, withhold, or permanently discontinue LYTGOBI based on duration and severity of hyperphosphatemia. Embryo-fetal Toxicity: LYTGOBI can cause fetal harm. Advise pregnant women of the potential risk to the fetus. Advise female patients of reproductive potential, and males with female partners of reproductive potential, to use effective contraception during treatment with LYTGOBI and for 1 week after the last dose. ADVERSE REACTIONS Serious adverse reactions occurred in 39% of patients receiving LYTGOBI, and in ≥2% of patients included pyrexia, gastrointestinal hemorrhage, ascites, musculoskeletal pain, and bile duct obstruction. The most common adverse reactions (≥20%) were nail toxicity, musculoskeletal pain, constipation, diarrhea, fatigue, dry mouth, alopecia, stomatitis, abdominal pain, dry skin, arthralgia, dysgeusia, dry eye, nausea, decreased appetite, urinary tract infection, palmar-plantar erythrodysesthesia syndrome, and vomiting. The most common laboratory abnormalities (≥20%) were increased phosphate, increased creatinine, decreased hemoglobin, increased glucose, increased calcium, decreased sodium, decreased phosphate, increased alanine aminotransferase, increased alkaline phosphatase, decreased lymphocytes, increased aspartate aminotransferase, decreased platelets, increased activated partial thromboplastin time, decreased leukocytes, decreased albumin, decreased neutrophils, increased creatine kinase, increased bilirubin, decreased glucose, increased prothrombin international normalized ratio, and decreased potassium. DRUG INTERACTIONS Dual P-gp and Strong CYP3A Inhibitors: Avoid concomitant use of drugs that are dual P-gp and strong CYP3A inhibitors. Dual P-gp and Strong CYP3A Inducers: Avoid concomitant use of drugs that are dual P-gp and strong CYP3A inducers. USE IN SPECIFIC POPULATIONS Lactation: Because of the potential for serious adverse reactions from LYTGOBI in breastfed children, advise women not to breastfeed during treatment and for 1 week after the last dose. Please see accompanying full Prescribing Information for complete details. For more information, visit About Taiho Oncology, Inc. The mission of Taiho Oncology, Inc. is to improve the lives of patients with cancer, their families and their caregivers. The company specializes in the development of orally administered anti-cancer agents and markets these medicines for a range of tumor types in the U.S. Taiho Oncology's growing pipeline of antimetabolic and selectively targeted anti-cancer agents is led by a world-class clinical development organization. Taiho Oncology is a subsidiary of Taiho Pharmaceutical Co., Ltd. which is part of Otsuka Holdings Co., Ltd. Taiho Oncology is headquartered in Princeton, New Jersey and oversees its parent company's European and Canadian operations, which are located in Zug, Switzerland and Oakville, Ontario, Canada. For more information, visit LYTGOBI is a registered trademark of Taiho Pharmaceutical Co., Ltd. *FGFR Oral SElective Novel Inhibitor X [across] tumors Taiho Oncology Media Contact: Judy Kay Moore Taiho Oncology, Inc. 574-526-2369 [email protected] SOURCE Taiho Oncology, Inc.