On May 8, 2017 GlycoMimetics, Inc. (NASDAQ: GLYC) reported progress on its clinical development programs and its financial results for the first quarter ended March 31, 2017 (Filing, Q1, GlycoMimetics, 2017, MAY 8, 2017, View Source [SID1234518898]).

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"In the first quarter of 2017, GlycoMimetics delivered on its plan to provide updates on both data and the status of its ongoing pipeline programs. The acceptance of our clinical and preclinical abstracts for presentation at key oncology congresses, including AACR (Free AACR Whitepaper) and more recently, ASCO (Free ASCO Whitepaper), reinforces our enthusiasm for the GMI-1271 and GMI-1359 programs, and demonstrates to the scientific and physician communities the relevance of our work to address unmet medical needs in a novel way. As we look forward to the remainder of 2017, our plan is to build on this progress with further data updates: at the Annual ASCO (Free ASCO Whitepaper) meeting in Chicago followed by the European Hematology Association (EHA) (Free EHA Whitepaper) meeting, both before the end of the second quarter in June. Additionally, we can report that the Phase 3 program to evaluate rivipansel for vaso-occlusive sickle cell crisis, according to our partner Pfizer, remains on track for completion in the second half of 2018, " said Rachel King, GlycoMimetics’ Chief Executive Officer.

Company management will host a conference call on Thursday, May 18, 2017 at 8:30 a.m. Eastern time to provide a clinical data update from the abstracts for the upcoming ASCO (Free ASCO Whitepaper) conference. A question and answer session with the GlycoMimetics team will follow the company’s remarks. The call can be accessed by dialing (844) 413-7154 (U.S. and Canada) or (216) 562-0466 (international) and entering passcode 4110139. To access the live audio webcast, or the subsequent archived recording, visit the "Investors – Events & Presentations" section of the GlycoMimetics website at www.glycomimetics.com. The webcast will be recorded and available for replay on the GlycoMimetics website for 30 days following the call.

Key Operational Highlights for the First Quarter of 2017:
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The first of two patient cohorts in the Phase 2 portion of the AML trial of GMI-1271 has completed enrollment. This cohort is comprised of 25 patients 60 years of age or older with newly diagnosed AML. The study is designed to evaluate the potential of GMI-1271, GlycoMimetics’ E-selectin antagonist drug candidate, in combination with chemotherapy, as a treatment for patients with both newly diagnosed and relapsed/refractory AML. Enrollment in the study’s second cohort is expected to complete in the middle of this year. The two arms combined will enroll a total of about 90 patients.
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Pre-clinical research supporting the potential of two of its drug candidates, GMI-1271 and GMI-1359, against multiple myeloma was shared via an oral presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2017. Combination therapy of carfilzomib with GMI-1271 or GMI-1359 prolonged survival of mice with multiple myeloma over treatment with carfilzomib alone.
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The company announced that it will provide an update on clinical data from its Phase 1/2 study of GMI-1271 in AML at the 2017 American Society for Clinical Oncology in Chicago. GMI-1271 is an antagonist of E-selectin, for which prior clinical data has shown an emerging and differentiated potential efficacy and safety profile.


First Quarter 2017 Financial Results:

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Cash position: As of March 31, 2017, GlycoMimetics had cash and cash equivalents of $34.6 million as compared to $40.0 million as of December 31, 2016. Subsequent to March 31, 2017, the Company has raised an additional $3.8 million in net proceeds under the at-the-market facility.

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R&D Expenses: The company’s research and development expenses increased to $5.9 million for the quarter ended March 31, 2017 as compared to $5.5 million for the first quarter of 2016. The increase was due to on-going costs associated with the clinical trials for GMI-1271 in AML and MM, partially offset by a decrease in expenses related to manufacturing and process development for GMI-1271.

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G&A Expenses: The company’s general and administrative expenses remained at $2.1 million for both the quarters ended March 31, 2017 and 2016.

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Shares Outstanding: Shares outstanding as of March 31, 2017 were 23,855,934.

About GMI-1271
GMI-1271 is designed to block E-selectin (an adhesion molecule on cells in the bone marrow) from binding with blood cancer cells as a targeted approach to disrupting well-established mechanisms of leukemic cell resistance within the bone marrow microenvironment. Preclinical research points to the drug’s potential role in moving cancerous cells out of the protective environment of the bone marrow where they hide and escape the effects of chemotherapy. In preclinical studies using animal models of AML, the results of which were presented at ASH (Free ASH Whitepaper) meetings, GMI-1271 was also associated with a reduction of chemotherapy-induced neutropenia and chemotherapy-induced mucositis.
About GMI-1359
GMI-1359 is designed to simultaneously inhibit both E-selectin and CXCR4. E-selectin and CXCR4 are both adhesion molecules that keep cancer cells in the bone marrow. Preclinical studies indicate that targeting both E-selectin and CXCR4 with a single compound could improve efficacy in the treatment of cancers that involve the bone marrow such as AML and MM.

On May 8, 2017 DelMar Pharmaceuticals (Nasdaq: DMPI) ("DelMar" and the "Company"), a biopharmaceutical company focused on developing new cancer therapies, reported new mechanism of action (MOA) data for its anti-cancer product candidate, VAL-083 (dianhydrogalactitol), a "first-in-class" small-molecule DNA-targeting agent in temozolomide (Temodar)-resistant GBM, at the World Federation of Neuro-Oncology Societies (WFNOS) (Press release, DelMar Pharmaceuticals, MAY 8, 2017, View Source [SID1234518897]).

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The Company presented two posters at the Quadrennial session of the WFNOS Conference in Zurich, Switzerland.

The titles and summaries of the posters are as follows:

Abstract 1: Distinct mechanism of action of dianhydrogalactitol (VAL-083) overcomes chemoresistance in glioblastoma. Zhai et al, 2017.

It has been previously demonstrated, both preclinically and in the clinic, that VAL-083 is active in temozolomide-resistant GBM. Glioblastoma cells are known to become refractory to treatment because they are able to repair the DNA damage caused by temozolomide using the MGMT* enzyme and the MMR** family of enzymes. While temozolomide is inactive in GBM cells where MGMT is functional, it has already been demonstrated that the activity of VAL-083 is unaffected by the MGMT status of a cell and hence VAL-083 remains active, even when temozolomide has failed.

The authors now show that VAL-083 is not only able to circumvent the MGMT pathway but is also able to override the secondary temozolomide resistance mechanism seen in GBM—MMR DNA repair. In cancer cell-lines VAL-083 is able to induce DNA damage and resultant cell apoptosis even when MMR enzymes (MLH-1 and MSH-2) are made constitutively active.

Taken together, these data provide preclinical evidence, and support the clinical rationale, that VAL-083 should be studied as a front-line therapy for GBM patients in whom active MGMT and MMR pathways will result in chemoresistance to temozolomide.

These results also add to the growing evidence that temozolomide may only be a viable front-line treatment in the 1/3 of GBM patients for whom biomarker data reveal inactive MGMT and MMR enzymes. VAL-083, whose activity is independent of, and agnostic to, the MGMT and MMR activity, may in fact be a superior alternative.

Abstract 2: Clinical trials of VAL-083 in patients with chemoresistant glioblastoma. Bacha et al, 2017.

In this poster the authors review historic clinical trials of VAL-083 run by the National Cancer Institute and the modern dose-finding trials conducted by DelMar (ASCO 2016) to provide the rationale for the ongoing and new clinical development of VAL-083 in GBM. This topic was also the recent subject of a contributed editorial by CEO Jeff Bacha and CSO Dennis Brown for Life Science Leader, entitled Cancer Breakthroughs: A Look to the Past Can be a Look to the Future.

DelMar has announced plans to investigate VAL-083 in Phase 2 and Phase 3 clinical trials in recurrent and newly diagnosed GBM. A pivotal randomized, controlled Phase 3 Study in Temozolomide-Avastin Recurrent GBM ("STAR-3") will evaluate the overall survival of VAL-083 versus salvage chemotherapy for GBM patients who have previously failed both temozolomide and bevacizumab (Avastin) and for whom there exists no approved treatment option. Should VAL-083 show a survival benefit in this moribund, recalcitrant population, it could revolutionize the GBM treatment landscape. A Phase 2 study of VAL-083 at MD Anderson Cancer Center is currently enrolling second-line GBM patients who have failed front-line temozolomide and test positive for MGMT. Finally, a Phase 2 trial enrolling MGMT-expressing front-line GBM patients to be treated with VAL-083 in lieu of temozolomide has the potential to introduce biomarker testing into the GBM treatment paradigm to determine which patients will receive temozolomide and VAL-083, respectively, based on their MGMT expression status.

*MGMT= O6-Methyl Guanine DNA-Methyl Transferase **MMR=mismatch repair

About VAL-083

VAL-083 is a "first-in-class," small-molecule chemotherapeutic that demonstrated clinical activity against a range of cancers including GBM in historical clinical trials sponsored by the U.S. National Cancer Institutes (NCI). DelMar has demonstrated that VAL-083’s anti-tumor activity against GBM is unaffected by the expression of MGMT and MMR in vitro. Further details can be found at View Source

VAL-083 has received an orphan drug designation in Europe for the treatment of malignant gliomas and the U.S. FDA Office of Orphan Products has granted an orphan designation to VAL-083 for the treatment of glioma, medulloblastoma and ovarian cancer. Based on historic clinical trials run by the NCI, the modern Phase 1/2 dose finding trial run by DelMar in GBM (ASCO 2016), and recent guidance from the FDA, the Company has embarked on Phase 2 or 3 trials for VAL-083 across recurrent and newly diagnosed GBM. DelMar has announced plans to advance VAL-083 into a pivotal randomized multi-center Phase 3 clinical trial for the treatment of bevacizumab-failed GBM, a Phase 2 trial (with MD Anderson Cancer Center) in first recurrence GBM patients prior to bevacizumab therapy, and into a separate international Phase 2 trial for newly diagnosed MGMT-unmethylated GBM. DelMar believes that data from its clinical trials, if successful, will form the basis of a new treatment paradigm for the vast majority of GBM patients whose tumors exhibit features that make them unlikely to respond to currently available therapies.

About Glioblastoma Multiforme (GBM)

GBM is the most common and aggressive primary brain cancer. Current standard of care includes surgery, radiation and treatment with temozolomide (TMZ), however nearly all tumors recur and the prognosis for recurrent GBM is dismal. Most GBM tumors have unmethylated promoter status for MGMT. Second-line treatment with anti-angiogenic agent bevacizumab has not improved overall survival (OS) and 5-year survival is less than 3%. VAL-083 (dianhydrogalactitol) is a first-in-class bi-functional DNA-targeting agent that induces interstrand DNA cross-links at the N7-position of guanine leading to DNA double-strand breaks and cell death in GBM cell lines and GBM cancer stem cells, independent of MGMT or MMR status in vitro. VAL-083 readily crosses the blood-brain barrier and accumulates in brain tumor tissue. Our recent Phase 1/2 clinical trial in recurrent GBM patients failing both TMZ and bevacizumab, suggested that VAL-083 offers clinically meaningful survival benefits for patients with recurrent GBM and pinpointed a new dosing regimen (40 mg/m2/d on days 1,2,3 of a 21-day cycle) which was well-tolerated and was selected for study in subsequent GBM trials. These trials include, i) an ongoing single-arm, biomarker driven, Phase 2 study to determine if VAL-083 treatment of MGMT-unmethylated adult GBM patients at first recurrence/progression, prior to bevacizumab improves overall survival, compared to historical control with lomustine (clinicaltrials.gov identifier: NCT02717962). ii) A pivotal Phase 3 study in recurrent GBM after failing both TMZ and bevacizumab. The control arm will consist of a limited number of salvage chemotherapies currently used in bevacizumab-failed GBM. If successful, this study will serve as the basis for a New Drug Application (NDA) submission for VAL-083. iii) A single arm, biomarker driven, Phase 2 study to confirm the tolerability and efficacy of VAL-083 in combination with radiotherapy in newly diagnosed MGMT-unmethylated GBM patients whose tumors are known to express high MGMT levels. The results of these studies may support a new treatment paradigm in chemotherapeutic regimens for the treatment of GBM.

On May 8, 2017 Oregon Health & Science University (OHSU) and Aptose Biosciences Inc. (NASDAQ:APTO) (TSX:APS) announced the presentation of preclinical data demonstrating that CG’806, a highly potent pan-FLT3/BTK inhibitor, kills malignant cells in samples from patients with various hematologic malignancies (Press release, Aptose Biosciences, MAY 8, 2017, View Source [SID1234518894]). The data were presented in a poster on Sunday, May 7 at the 2017 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Conference Hematologic Malignancies: Translating Discoveries to Novel Therapies, held May 6-9 in Boston, MA.

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The poster, entitled CG’806, a First-in-Class FLT3/BTK Inhibitor, Exhibits Potent Activity against AML Patient Samples with Mutant or Wild-Type FLT3, as well as Other Hematologic Malignancy Subtypes, demonstrated the broad potency of CG’806 against various hematologic malignancy cell lines and patient primary bone marrow specimens. In addition, data for CG’806 indicated greater potency of CG’806 when compared to other non-proprietary competitive agents in acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), including the bromodomain inhibitors OTX-015 and JQ-1, and the FLT3 inhibitor quizartinib.

"The analyses of CG’806 against primary hematologic malignancy patient samples and cultured cell lines show evidence of potent and broad drug activity in AML and other disease subtypes and support further development of this agent for hematologic malignancies," said Stephen E. Kurtz, Ph.D., lead author and Research Assistant Professor at the OHSU Knight Cancer Institute.

"These findings further strengthen our commitment to develop CG’806 as a targeted treatment for AML and other hematologic malignancies," commented William G. Rice, Ph.D., Chairman and Chief Executive Officer of Aptose. "We are actively preparing ’806 for clinical studies and look forward to filing an IND and taking the molecule into patients as soon as possible."

Through the Beat AML Initiative, primary patient mononuclear cells were derived from 82 patients diagnosed with AML. Primary samples were also collected from patients with myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN, n=15), acute lymphoblastic leukemia (ALL, n=17), and chronic lymphocytic leukemia (CLL, n=58). Sensitivity to CG’806 was evaluated across a range of concentrations after a 72-hour treatment. IC50 values were calculated as a measure of drug sensitivity and compared to other agents.

Across the four general subtypes of hematologic malignancies in the dataset, there was broad sensitivity to CG’806, with 59% (48/82) of AML, 29% (5/17) of ALL, 53% (8/15) of MDS/MPN, and 40% (23/58) of CLL cases exhibiting an IC50 of less than 100 nM. Primary AML and CLL cells were sensitive to CG’806 with median IC50 values of 70 nM and 220 nM, respectively. Among the 38 tested AML samples with known FLT3 mutational status, the FLT3-ITD+ AML samples tended to have enhanced sensitivity to CG’806 (median IC50 = 20 nM, n=8) relative to the FLT3-WT samples (median IC50 = 120 nM, n=30). CG’806 also exerted potent anti-proliferative activity against human AML, B-ALL, mantle cell lymphoma, Burkitt’s lymphoma, and diffuse large B-cell lymphoma cell lines. In comparison to the FLT3 inhibitor quizartinib, CG’806 completely inhibited phosphorylation of FLT3 and STAT5 in MV4-11 cells, whereas quizartinib only partially inhibited their phosphorylation.

The presentation will be published in the AACR (Free AACR Whitepaper) Hematologic Malignancies Conference Proceedings. The poster can also be accessed here or at the Publications & Presentations section of the Aptose website, www.aptose.com.

About CG’806
CG’806 is a once-daily, oral, first-in-class pan-FLT3/BTK inhibitor. This small molecule demonstrates potent inhibition of mutant forms of FLT3 (including internal tandem duplication, or ITD, and mutations of the receptor tyrosine kinase domain and gatekeeper region), eliminates AML tumors in the absence of toxicity in murine xenograft models, and represents a potential best-in-class therapeutic for patients with FLT3-driven AML. Likewise, CG’806 demonstrates potent, non-covalent inhibition of the Cys481Ser mutant of the BTK enzyme, as well as other oncogenic kinases operative in B cell malignancies, suggesting CG’806 may be developed for CLL and MCL patients that are resistant/refractory/intolerant to covalent BTK inhibitors.

About the Beat AML Initiative
The Leukemia & Lymphoma Society and the Knight Cancer Institute at Oregon Health & Science University (OHSU) — joined by partnering medical institutions and industry collaborators — are performing groundbreaking research to better understand acute myeloid leukemia (AML). Led by researchers at the Knight Cancer Institute, Beat AML collects samples from participating AML patients treated at 11 academic medical centers across the U.S. Knight Cancer Institute researchers conduct deep genomic sequencing analyses on those samples to create a profile of the possible genetic drivers of AML. Researchers also test the sensitivity of patients’ leukemic cells to a diverse panel of targeted therapies and novel combination regimens. The goal is to eventually match patients with treatments that precisely target their leukemia for durable remissions in AML.

On May 8, 2017 Immunocore Limited, the world’s leading TCR company developing biological drugs to treat cancer, infectious diseases and autoimmune diseases, reported that it has identified a lead compound in its second discovery programme with GSK (Press release, Immunocore, MAY 8, 2017, View Source [SID1234518893]). This novel ImmTAC lead molecule is relevant in a number of cancers including triple negative breast cancers, oesophageal, gastric and ovarian cancers. The identification of this new ImmTAC has triggered an undisclosed milestone payment to Immunocore.

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Immunocore is now working on two ImmTAC programmes under the discovery collaboration agreement with GSK. The first ImmTAC programme under Immunocore’s GSK collaboration is on track to be submitted as an IND this year and will enter Phase I clinical studies during early 2018, with potential application in Non-Small Cell Lung Cancer (NSCLC), bladder cancer, synovial sarcoma, melanoma and ovarian cancer.

Immunocore and GSK announced their collaboration in 2013, and Immunocore will receive up to a total of £142 million in pre-clinical milestone payments. In addition, for each product that reaches the market, up to £200 million is due to Immunocore in development and commercial milestone payments, plus up to double digit royalties. Immunocore will be responsible for all pre-clinical development and for the initial clinical trial in patients for the first two programmes. GSK will be responsible for the remaining development and commercialisation of the products.

Dr Bent Jakobsen, Chief Scientific Officer at Immunocore, commented: "Our discovery collaboration with GSK is generating novel ImmTAC molecules which are relevant across multiple solid tumours and the disease targets are all intracellularly located, which are hard for other biologic platforms to reach. Our ImmTAC technology is continuing to demonstrate its versatility across a wide range of cancer types showing an ability to tackle solid ‘cold’, low mutation rate tumours – the majority of tumours and across other diseases. We are growing increasingly confident about our opportunity to help patients with some of the most intractable cancers and major diseases."

Dr Axel Hoos, Senior Vice President Therapeutic Area Head, Oncology R&D Head, at GSK, added: "Our collaboration with Immunocore is progressing extremely well and we have identified novel and promising ImmTAC molecules with potential utility across a broad range of cancer types. We look forward to continued progress in both programmes."

On May 8, 2017 Epizyme, Inc. (NASDAQ:EPZM), a clinical-stage biopharmaceutical company creating novel epigenetic therapies, reported operating results for the first quarter 2017 and reiterated timelines for its upcoming data presentations (Press release, Epizyme, MAY 8, 2017, View Source [SID1234518890]).

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Upcoming Tazemetostat Clinical Data Presentations

Phase 2 in Molecularly Defined Solid Tumors: Interim efficacy and safety data from study cohorts in Epizyme’s ongoing Phase 2 clinical trial of tazemetostat in adult patients with molecularly defined solid tumors that have reached futility assessment by the Independent Data Monitoring Committee will be reported in two poster presentations at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting taking place June 2-6, 2017 in Chicago. The Company will host a conference call to discuss the data on Thursday, May 18 at 8:30 a.m. ET, after ASCO (Free ASCO Whitepaper) abstracts have been released.

To participate in the conference call, please dial (877) 844-6886 (domestic) or (970) 315-0315 (international) and refer to conference ID 12186629. The webcast, and accompanying slides for the call, will be accessible under "Events and Presentations" in the Investor Relations section of the Company’s website at www.epizyme.com.

Phase 2 in Non-Hodgkin Lymphoma: Interim efficacy and safety data from all five monotherapy study cohorts in Epizyme’s ongoing Phase 2 study of tazemetostat in patients with relapsed or refractory follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) has been selected for a plenary session on Wednesday, June 14, 2017 at 2:00 p.m. CET (8:00 a.m. ET) at the International Conference on Malignant Lymphoma (ICML) in Lugano, Switzerland. Data from a 62-gene panel biomarker study of tazemetostat in patients with NHL will also be presented in a poster session during ICML. The Company plans to hold a conference call to discuss these clinical findings on Wednesday, June 14 at 10:30 a.m. ET.

To participate in the conference call, please dial (877) 844-6886 (domestic) or (970) 315-0315 (international) and refer to conference ID 15855261. The webcast, and accompanying slides for the call, will be accessible under "Events and Presentations" in the Investor Relations section of the Company’s website at www.epizyme.com.
"Already in 2017, we have made progress in our novel epigenetic pipeline, led by tazemetostat," stated Robert Bazemore, president and chief executive officer. "We have continued to advance tazemetostat in multiple clinical trials in a range of solid tumors and hematological malignancies, and as both a monotherapy and in combination with other anti-cancer agents. We look forward to reporting interim data from our Phase 2 study in molecularly defined solid tumors in our conference call next week and from our Phase 2 study in relapsed or refractory FL and DLBCL in June."

Recent Achievements

In May 2017, the Company earned a $10 million milestone payment from GlaxoSmithKline (GSK). The milestone payment follows GSK’s initiation of GLP toxicology studies for a first-in-class methyltransferase inhibitor discovered by Epizyme and licensed to GSK.
In April 2017, the U.S. Food and Drug Administration (FDA) granted Fast Track designation to tazemetostat for the treatment of patients with relapsed or refractory FL, including patients whose tumors have wild type EZH2 or EZH2 activating mutations. Fast Track designation is intended to provide expedited processes for the development and FDA review of drugs that may reduce development time and costs associated with bringing a drug to market.
In March 2017, Epizyme initiated clinical investigation of tazemetostat in combination with prednisolone in relapsed or refractory patients with DLBCL, based on observed preclinical synergy of the agents. This combination regimen is being conducted as the sixth cohort in the ongoing Phase 2 NHL study.
In January 2017, Epizyme completed enrollment of all wild type EZH2 cohorts in its ongoing Phase 2 study of tazemetostat in patients with relapsed or refractory FL and DLBCL.
First Quarter 2017 Financial Results

Cash Position: Cash, cash equivalents and marketable securities were $211.2 million as of March 31, 2017, as compared to $242.2 million as of December 31, 2016.
Revenue: No revenue was recognized in the first quarter of 2017, compared to $0.5 million for the first quarter of 2016.
R&D Expenses: Research and development (R&D) expenses were $24.7 million for the first quarter of 2017, compared to $17.7 million for the first quarter of 2016. The increase is primarily due to the expansion of the tazemetostat clinical program and advancement of our proprietary research pipeline.
G&A Expenses: General and administrative (G&A) expenses were $8.3 million for the first quarter of 2017, compared to $5.8 million for the first quarter of 2016. The increase is primarily due to higher pre-commercial, intellectual property, business development and product planning expenses.
Net Loss: Net loss was $32.5 million for the first quarter of 2017, compared to $22.9 million for the first quarter of 2016.
2017 Guidance
Epizyme believes, based on its current operating plan, that its cash, cash equivalents and marketable securities of $211.2 million as of March 31, 2017 will be sufficient to fund the Company’s planned operations into at least the third quarter of 2018.

About the Tazemetostat Clinical Trial Program
Tazemetostat, a first-in-class EZH2 inhibitor, is currently being studied in ongoing Phase 2 programs in both follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) forms of non-Hodgkin lymphoma; certain molecularly defined solid tumors, including epithelioid sarcoma and other INI1-negative tumors; and mesothelioma, as well as in combination studies in DLBCL. Tazemetostat has been granted Fast Track designation by the U.S. Food and Drug Administration for the treatment of patients with relapsed or refractory FL, either wild type EZH2 or with EZH2 activating mutations, and for relapsed or refractory DLBCL with EZH2 activating mutations, as well as Orphan Drug designation for malignant rhabdoid tumors.