On December 5, 2016 TG Therapeutics, Inc. (NASDAQ:TGTX), reported the presentation of two preclinical data sets, one oral presentation and one poster presentation, for TGR-1202, the Company’s once-daily PI3K delta inhibitor, at the 58th American Society of Hematology (ASH) (Free ASH Whitepaper) annual meeting in San Diego, California (Press release, TG Therapeutics, DEC 5, 2016, View Source [SID1234516932]).

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Michael S. Weiss, the Company’s Executive Chairman and Interim Chief Executive Officer, stated, "We want to thank the teams at Columbia and Moffitt for their extensive laboratory work on TGR-1202 to better understand the mechanism of action and impact on the immune system. The preclinical data they have generated helps to better explain and perhaps offer a rationale for the differentiated safety profile seen with TGR-1202 as compared to earlier generation PI3K delta inhibitors. We believe these preclinical findings along with the robust safety and efficacy data we have observed in the clinic, support our belief that TGR-1202 is a differentiated best in class PI3K delta inhibitor. We look forward to continuing our research collaborations with Columbia and Moffitt and to presenting updated safety and efficacy data for TGR-1202 to further confirm its unique profile."

"Dr. Deng’s presentation today has really begun to shed some long-needed light on the important differences among the PI3K delta inhibitors. His work has identified that a novel kinase important in the PI3K pathway, CK-1epsilon, is uniquely inhibited by TGR-1202, which may explain the drug’s effects on c-Myc. These chemical differences may also help to explain the important immunologic differences in the safety profiles of these agents," stated Dr. Owen A. O’Connor, Professor of Medicine and Experimental Therapeutics, Director Lymphoid Malignancies at Columbia Presbyterian Medical Center.

The following summarizes the oral presentation and poster presentation which occurred yesterday:

Oral Presentation: Silencing c-Myc Translation as a Therapeutic Strategy through Targeting PI3K Delta and CK1 Epsilon in Hematological Malignancies (Abstract Number 291)

This oral presentation includes data from the manuscript titled, "Silencing c-Myc Translation as a Therapeutic Strategy through Targeting PI3K Delta and CK1 Epsilon in Hematological Malignancies," which was recently published in Blood, the Journal of the American Society of Hematology (ASH) (Free ASH Whitepaper). The presentation was delivered by Changchung Deng, MD, PhD of Columbia Presbyterian Medical Center and included the following highlights:

TGR-1202 and carfilzomib, but not combinations of other drugs in the same classes, synergistically inhibit c-Myc translation and c-Myc dependent gene transcription, by potently inhibiting phosphorylation of 4E-BP1;
TGR-1202 and carfilzomib synergistically induce apoptosis in lymphoma cells through targeting c-Myc, whereas the other combinations did not;
TGR-1202, but not idelalisib or duvelisib, was found to uniquely inhibit casein kinase-1 (CK1) epsilon; and
Based on this extensive preclinical work, the Company recently announced the launch of a Phase 1/2 study to evaluate the safety and efficacy of TGR-1202 in combination with carfilzomib, in patients with relapsed or refractory lymphoma.
Poster Presentation: Modulation of T Cell Compartment in a Preclinical CLL Murine Model By a Selective PI3K Delta Inhibitor, TGR-1202 (Abstract Number 3236)

This poster presentation included preclinical data describing the differential regulation of human T-cells by TGR-1202 in a preclinical CLL murine model. Highlights from this poster include:

Both TGR-1202 and duvelisib oral administration demonstrated comparable efficacy by reducing CLL burden over time in leukemic mice;
TGR-1202 and duvelisib both targeted the T cell population in vivo, however:
TGR-1202 relatively maintained the number of Tregs and Th17 cells and expression of functional markers on Tregs compared to duvelisib treatment in vivo and ex vivo; and
Duvelisib resulted in greater disruption of Treg/Th17 ratio compared to TGR-1202 in vivo, which may have implications for occurrence of autoimmune-like organ toxicity.
PRESENTATION DETAILS:
Copies of the above referenced presentations are available on the Company’s website at www.tgtherapeutics.com, located on the Publications page.

TG THERAPEUTICS INVESTOR & ANALYST EVENT DETAILS:
TG Therapeutics will also host an investor and analyst reception on Monday, December 5th, 2016 beginning at 8:00pm PT. The event will take place at the Marriott Gaslamp, in San Diego, California, in the Presidio AB Ballroom.
NOTE: This event will be webcast live and will be available on the Events page, located within the Investors & Media section of the Company’s website at www.tgtherapeutics.com, as well as archived for future review. This event will also be broadcast via conference call. In order to access the conference line, please call 1-877-407-8029 (U.S.), 1-201-689-8029 (outside the U.S.), and reference Conference Title: TG Therapeutics 2016 Investor & Analyst Event.

On December 5, 2016 Seattle Genetics, Inc. (Nasdaq: SGEN), a global biotechnology company, reported three oral data presentations on vadastuximab talirine (SGN-CD33A; 33A) in patients with acute myeloid leukemia (AML) at the 58th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition taking place in San Diego, California, December 3-6, 2016 (Press release, Seattle Genetics, DEC 5, 2016, View Source;p=RssLanding&cat=news&id=2227547 [SID1234516931]). The data included updated results from an ongoing phase 1 clinical trial evaluating 33A in combination with hypomethylating agents (HMAs; azacitidine, decitabine) in frontline older AML patients. Further oral presentations focused on results from phase 1 clinical trials evaluating 33A in three distinct settings, including 1) as monotherapy in newly diagnosed older AML patients, 2) in combination with high-dose cytarabine for younger AML patients in first remission and 3) as monotherapy maintenance for younger AML patients who have completed frontline therapy or after allogeneic stem cell transplant. 33A is an investigational antibody-drug conjugate (ADC) targeted to CD33, a protein which is expressed on leukemic cells in nearly all AML patients.

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Seattle Genetics is broadly evaluating 33A across multiple lines of therapy in patients with myeloid malignancies. In addition to the clinical trials presented at ASH (Free ASH Whitepaper) this year, 33A is currently being evaluated in combination with HMAs in the ongoing global phase 3 CASCADE study. This trial is randomized, double-blind, and being conducted at multiple centers globally to evaluate if 33A in combination with azacitidine or decitabine can extend overall survival compared to azacitidine or decitabine alone in approximately 500 older patients with newly diagnosed AML. Additional phase 1 and 2 clinical trials for frontline younger AML and frontline myelodysplastic syndrome (MDS) are also underway. More information about 33A and ongoing clinical trials can be found at www.ADC-CD33.com.

"We are pleased with the growing body of data demonstrating that vadastuximab talirine, also known as 33A, has a promising overall tolerability and activity profile in clinical trials for patients with AML," said Jonathan Drachman, M.D., Chief Medical Officer and Executive Vice President, Research and Development at Seattle Genetics. "We are committed to improving the therapeutic options for AML patients through innovative, targeted approaches. Our most advanced 33A clinical study, CASCADE, is a randomized phase 3 trial designed to test 33A in combination with hypomethylating agents, or HMAs, in approximately 500 older patients with newly diagnosed AML. Based on the encouraging data presented at ASH (Free ASH Whitepaper), we believe 33A has the potential for clinical development in multiple AML settings, with the goal of providing new treatment options for patients struggling with this aggressive and life-threatening disease."

"AML therapy has not meaningfully changed over the past 40 years, and there is a dire need for improved treatment options. Older AML patients have a particularly poor prognosis with the standard of care, hypomethylating agents or HMAs," said Amir Fathi, M.D., Massachusetts General Hospital Cancer Center. "I am pleased with the balance of activity and tolerability we have observed in phase 1 clinical trials evaluating 33A both as monotherapy and combination therapy in AML patients. For older patients with newly diagnosed AML, the 73 percent remission rate of 33A in combination with HMAs, with 50 percent of those patients negative for minimal residual disease, signals promise in improving long-term outcomes."

The following data from the ongoing phase 1 studies evaluating 33A combination therapy or monotherapy in AML patients were presented:

Vadastuximab Talirine Plus Hypomethylating Agents: A Well-Tolerated Regimen with High Remission Rate in Frontline Older Patients With Acute Myeloid Leukemia (Abstract #591, oral presentation on Monday, December 5, 2016 at 7:30 a.m. PT)

Outcomes for AML patients who are older or ineligible to receive standard chemotherapy remain poor. HMAs are frequently used in this setting, but efficacy is limited. Updated results from an ongoing phase 1 study evaluating 33A in combination with HMAs (either azacitidine or decitabine) in newly diagnosed older AML patients were presented by Dr. Amir Fathi, Massachusetts General Hospital Cancer Center.

Data were reported from 53 frontline AML patients with a median age of 75 years and predominantly intermediate or adverse cytogenetic risk who had declined intensive therapy. Regarding additional poor-prognosis indicators, 42 percent of patients had evidence of underlying myelodysplasia, 11 percent had FLT3-mutated disease and 43 percent had secondary AML, which is AML that arises from prior chemotherapy, a pre-existing MDS or myeloproliferative disease. Key findings include:

Of 49 patients evaluable for response, complete remission (CR) or CR with incomplete platelet or neutrophil recovery (CRi) was observed in 36 patients (73 percent).
Remissions were observed in higher-risk patients, including 17 of 22 patients (77 percent) with secondary AML, five of five patients (100 percent) who were FLT3/ITD positive and 17 of 26 patients (65 percent) age 75 or older.
Eighteen of the 36 patients (50 percent) who achieved remission (CR or CRi) were negative for minimal residual disease (MRD), which means no cancer could be detected with a sensitive test.
With a median follow-up of 14.7 months, median overall survival for all patients was 11.3 months and 28 percent of patients remained alive and on study as of last follow-up. The 30- and 60-day mortality rates were two and eight percent, with no treatment-related deaths occurring during that time.
For patients who achieved MRD-negative remission, the median survival had not yet been reached.
The most common Grade 3 or 4 treatment-emergent adverse events occurring in 20 percent or more of patients were thrombocytopenia, febrile neutropenia, anemia and neutropenia.
The most common Grade 1 and 2 treatment-emergent adverse events occurring in 20 percent or more of patients were fatigue, nausea, constipation, peripheral edema and decreased appetite.
Vadastuximab Talirine Monotherapy in Older Patients with Treatment Naive CD33-Positive Acute Myeloid Leukemia (Abstract #590, oral presentation on Monday, December 5, 2016 at 7:15 a.m. PT)

Interim results from 93 patients in the ongoing phase 1 study evaluating 33A monotherapy in AML patients were previously presented at the 2015 ASH (Free ASH Whitepaper) Annual Meeting. New results describing the safety and activity of the recommended 33A monotherapy dose of 40 micrograms per kilogram (mcg/kg) in an expansion cohort of treatment-naïve older AML patients were presented by Dr. Anjali Advani, Cleveland Clinic.

Data were reported from 27 treatment-naïve older AML patients with a median age of 74 years and intermediate or adverse cytogenetic risk of 70 percent and 26 percent, respectively. Regarding additional poor-prognosis indicators, 48 percent of patients had evidence of underlying myelodysplasia and 22 percent had FLT3 mutated disease. Key findings include:

Of the 26 patients evaluable for response, remission (CR or CRi) was observed in 15 patients (58 percent), with a median time to remission of 1.4 months.
Forty-three percent of patients who achieved remission were MRD negative.
Responses were observed in higher-risk patients, with remissions achieved in seven of 12 patients (58 percent) with underlying myelodysplasia and three of four patients (75 percent) who were positive for FLT3/ITD.
The 30- and 60-day mortality rates were zero and 15 percent, respectively. The median overall survival for all patients was seven months.
The most common Grade 3 or higher treatment-emergent adverse events occurring in 20 percent or more of patients were thrombocytopenia, febrile neutropenia and anemia.
The most common Grade 1 and 2 treatment-emergent adverse events occurring in 20 percent or more of patients were peripheral edema, decreased appetite, fatigue, diarrhea and dizziness.
A Phase 1b Study of Vadastuximab Talirine as Maintenance and in Combination with Standard Consolidation for Patients with Acute Myeloid Leukemia (Abstract #340, oral presentation on Sunday, December 4, 2016 at 10:15 a.m. PT)

Interim results from an ongoing phase 1b study evaluating 33A in the AML post-remission setting, as a single agent for maintenance therapy or in combination with consolidation therapy (high-dose cytarabine; HiDAC), were presented by Dr. Jay Yang, Karmanos Cancer Institute.

About Acute Myeloid Leukemia

Acute myeloid leukemia, also called acute myelocytic leukemia or AML, is an aggressive cancer of the bone marrow and blood that progresses rapidly without treatment. Cancerous cells called leukemic blasts multiply and crowd out normal cells in the bone marrow and interfere with normal blood cell production leading to anemia, infection, and bleeding. According to the SEER database and Kantar Health Sciences, in 2016 approximately 33,000 new cases of AML (mostly in adults) will be diagnosed in the U.S. and Europe. In the U.S. alone, nearly 10,500 deaths will occur from AML this year. Treatment options for AML have remained virtually unchanged for nearly 40 years and frontline treatment consists primarily of chemotherapy. A subset of patients (typically those over 60 years of age) cannot tolerate such therapy and are typically given lower intensity therapies agents, supportive care, or are recommended for clinical trials.

About Vadastuximab Talirine (SGN-CD33A)

Vadastuximab talirine (SGN-CD33A; 33A) is a novel investigational ADC targeted to CD33 utilizing Seattle Genetics’ proprietary ADC technology. CD33 is expressed on most AML and MDS blast cells. The CD33 engineered cysteine antibody is stably linked to a highly potent DNA binding agent called a pyrrolobenzodiazepine (PBD) dimer via site-specific conjugation technology (EC-mAb). PBD dimers are significantly more potent than systemic chemotherapeutic drugs and the EC-mAb technology allows uniform drug-loading onto an ADC. The ADC is designed to be stable in the bloodstream and to release its potent cell-killing PBD agent upon internalization into CD33-expressing cells.

33A was granted Orphan Drug Designation by both the U.S. Food and Drug Administration (FDA) and the European Commission for the treatment of AML. FDA orphan drug designation is intended to encourage companies to develop therapies for the treatment of diseases that affect fewer than 200,000 individuals in the United States.

On December 5, 2016 Immune Design, a clinical-stage immunotherapy company focused on oncology, reported new data that highlight the broad product reach potential of both its Specific Antigen and Endogenous Antigen/Intratumoral immunization approaches (Press release, Immune Design, DEC 5, 2016, View Source [SID1234516927]).

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ZVexMulti offers the potential to create products that deliver multiple tumor antigens (conserved and/or neo-antigens) to dendritic cells (DCs) in vivo within the same product

Immune Design recently presented preclinical data at SITC (Free SITC Whitepaper) 2016 (Poster #195) showing that immunization with ZVexMulti (multi-genome ZVex) vectors expressing multiple antigens resulted in consistent induction of polyfunctional CD8 T cells against all delivered antigens, thereby overcoming the limitation of antigen competition. Moreover, immune responses were as high as, or higher than, those obtained by combining individually manufactured vectors, demonstrating the versatility and potency of ZVexMulti.

Immune Design scientists have also investigated the potential for ZVexMulti to deliver multiple MHC Class I and II putative neo-antigens in the CT.26 colon carcinoma model. Immune Design believes that ZVexMulti has the potential to deliver a significantly large number of neo-antigens, thus obviating the need for a proprietary predictive algorithm tools. These experiments were performed outside of the previously announced collaboration with Gritstone Oncology, which the two parties have agreed to terminate.

"These data collectively illustrate the range and flexibility of Immune Design’s product discovery platforms to target both conserved tumor antigens and neo-antigens," said Jan ter Meulen, MD, PhD, Chief Scientific Officer at Immune Design. "These approaches offer the potential to reach a broad patient population, while addressing some of the current limitations of other immunization approaches."

G100 ASH (Free ASH Whitepaper) data demonstrate eradication of lymphomas via synergy with local radiation

At the 58th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in San Diego, California, on Monday, December 5 at 6pm Pacific, Immune Design is presenting data (Abstract #4166, Session: 625, "Intratumoral G100 Rescues Radiation-Induced T Cell Depletion and Has Synergistic Anti-Tumor Effect with Local Irradiation in A20 Lymphoma") showing the synergistic effects of the G100 product candidate in combination with local radiation therapy in eradicating lymphomas in preclinical models. These data further support Immune Design’s ongoing randomized Phase 2 study in patients with follicular non-Hodgkin’s lymphoma (NHL).

The research, authored by Ramesh Rengan, Eric Ford and Jeffery L. Schwartz of the University of Washington Department of Radiation Oncology, and Hailing Lu, Jessica Hewitt, Frank Hsu and Jan ter Meulen of Immune Design, evaluated the immune response and therapeutic effects of intratumoral administration of G100 alone, local radiation alone and G100 and local radiation given in concomitant therapy in a preclinical model of lymphoma. Results of combination therapy demonstrated:

Synergistic antitumor effects in both injected as well as uninjected tumors (abscopal effects)
Synergistic induction of pro-inflammatory cytokine and chemokine environment, as well as induction of genes governing antigen processing and presentation
Increased infiltration of T cells, including both CD4 and CD8 T cells, in treated tumors
In contrast, tumors that received only radiation but no G100 had significantly decreased levels of T lymphocytes as compared to untreated tumors
"These findings highlight the potential beneficial effect that immunotherapy with G100 could provide when given with radiation by modulating the tumor microenvironment to generate a systemic, durable T-cell anti-tumor response," said Ramesh Rengan, M.D., Associate Professor, University of Washington Department of Radiation Oncology. "As shown in this model, G100 may hold potential as a treatment for lymphoma patients."

About ZVex and ZVexMulti

ZVex is Immune Design’s discovery platform, initially designed to deliver a single RNA tumor antigen selectively directly to the patient’s DCs to generate tumor antigen-specific polyclonal cytotoxic T cells (CTLs). ZVex is an engineered recombinant viral vector that selectively targets DCs in vivo to deliver any RNA gene of interest. Further development of this platform has yielded ZVexMulti, enabling Immune Design to deliver multiple RNA tumor antigens within the same product candidate.

About G100

G100 is a product candidate from Immune Design’s GLAASTM discovery platform. It is a synthetic small molecule toll-like receptor-4 (TLR-4) agonist, Glucopyranosyl Lipid A (GLA), formulated in a stable and oil emulsion. G100 is one of the molecules utilized in Immune Design’s intratumoral immune activation, or Endogenous Antigen, approach. It leverages the activation of the innate immune system, including DCs, in the tumor microenvironment to create a robust immune response against the tumor’s preexisting diverse set of antigens. A growing set of clinical and preclinical data have demonstrated the ability of G100 to activate existing tumor-infiltrating lymphocytes and promote antigen-presentation and the recruitment of T cells to the tumor to affect clinical outcome, as well as convert immunosuppressive M2-type tumor associated macrophages to a pro-inflammatory, M1-type.

On December 5, 2016 ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA), a rare cancer-focused innovative biotechnology company, reported clinical data on brigatinib, its investigational anaplastic lymphoma kinase (ALK) inhibitor, from the ongoing Phase 1/2 and pivotal ALTA trials in patients with ALK-positive (ALK+) non-small cell lung cancer (NSCLC) and intracranial central nervous system (CNS) metastases (Press release, Ariad, DEC 5, 2016, View Source;p=RssLanding&cat=news&id=2227425 [SID1234516925]). These data, being presented today at the International Association for the Study of Lung Cancer (IASLC) 17th World Conference on Lung Cancer (WCLC) being held in Vienna, showed that in patients with measurable brain metastases, the confirmed intracranial objective response rate (ORR) was 53 percent in the Phase 1/2 trial, and the confirmed intracranial ORR was 67 percent in Arm B (brigatinib 180 mg with seven-day lead-in at 90 mg once daily) in the ALTA trial. Median intracranial progression-free survival (PFS) in ALTA Arm B was 18.4 months.

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"Although crizotinib is initially effective in most patients with advanced ALK rearranged lung cancer, patients eventually develop resistance to crizotinib, often with new or progressive brain metastases," said presenting author Scott N. Gettinger, M.D., associate professor of medicine at Yale Cancer Center. "We are clearly encouraged by these data that demonstrate efficacy in the brain, with median intracranial PFS of over one and a half years, in patients with crizotinib refractory disease."

The ALTA Trial

The ALTA (ALK in Lung Cancer Trial of AP26113) trial enrolled 222 patients with ALK+ NSCLC who had been treated with and experienced disease progression on their most recent crizotinib therapy. Patients were randomized one-to-one to receive either 90 mg of brigatinib once per day (QD) (Arm A), or 180 mg QD with a seven-day lead-in at 90 mg QD (Arm B). In addition, patients were stratified by presence of brain metastases at baseline and best response to prior crizotinib therapy. Patient enrollment is complete, with the last patient enrolled in September 2015. Median follow-up in all patients with intracranial CNS metastases at baseline enrolled in the ALTA trial was 10.7 months as of May 31, 2016.

Phase 1/2 Study

The Phase 1/2 study of brigatinib included a dose-escalation portion that enrolled patients with advanced solid tumors, particularly those with NSCLC, who were either refractory to available therapies or had no standard treatment available to them. The Phase 2 portion of the trial includes five expansion cohorts. The trial enrolled 137 patients with 79 patients having ALK+ NSCLC. All but eight ALK+ NSCLC patients had failed prior crizotinib therapy. Patient enrollment in the trial is complete, with the last patient enrolled in July 2014. Median follow-up in ALK+ NSCLC patients with intracranial CNS metastases at baseline in the Phase 1/2 study was 24.9 months as of May 31, 2016.

Key Data from Oral Presentation on Patients with Baseline CNS Metastases from Phase 1/2 and ALTA Trials

Follow-up Data as of May 31, 2016; Last IRC Data in ALTA Trial was July 13, 2016, and Last Brain Scan in Phase 1/2 Trial was October 8, 2015

In the Phase 1/2 trial of brigatinib, 50/79 (63%) of ALK+ NSCLC patients had IRC-assessed baseline brain metastases. In the ALTA trial, 153/222 (69%) of ALK+ NSCLC patients had IRC-assessed baseline brain metastases. The efficacy analysis of Phase 1/2 trial data was based on an evaluable population (patients with at least one on-study brain scan, n=46), and the analysis of ALTA trial data was based on the intention-to-treat (ITT) population (n=153).
As of May 31, 2016, 42 percent and 55 percent of ALK+ NSCLC patients with brain metastases at baseline remained on study in the Phase 1/2 and ALTA populations respectively.
For patients with measurable brain lesions, the confirmed intracranial ORR was 53 percent (8/15) in the Phase 1/2 trial, and confirmed intracranial ORRs were 67 percent (12/18) in Arm B and 46 percent (12/26) in Arm A in the ALTA trial.
There were 31 patients in the Phase 1/2 trial with only non-measurable brain lesions, and of these, 35 percent had complete resolution of lesions. In ALTA, there were 55 patients in Arm B and 54 in Arm A with only non-measurable lesions; of these, 18 percent and seven percent of patients, respectively, had complete resolution of lesions.
For patients with any brain metastases at baseline:
Median duration of intracranial response in confirmed responders was 11.4 months in the Phase 1/2 trial (n=19); and was not yet reached in either arm of the ALTA trial (n=22 in Arm B and n=16 in Arm A).
Median intracranial PFS was 14.6 months in the Phase 1/2 trial (n=46); and 18.4 months (95% confidence interval [CI] 12.8 – not reached) and 15.6 months (95% CI 9.0-18.3 months) in ALTA Arm B and Arm A, respectively (n=73/n=80).
In the Phase 1/2 trial (n=46), for patients with any brain metastases at baseline, investigator-assessed whole-body ORR was 74 percent, median duration of response was 24 months and median PFS was 14.5 months. In ALTA (Arms B and A, respectively), for patients with any brain metastases at baseline, investigator-assessed whole-body ORR was 58 percent and 39 percent, median duration of response was not yet reached and 12 months, and median PFS was 12.9 months and 9.2 months.
In patients with any brain metastases at baseline in the ALTA trial, the most common treatment-emergent adverse events (AEs), grade 3 or higher (excluding neoplasm progression), were (n=151 treated; Arm B/A): increased creatine phosphokinase (CPK) (12%/1%), hypertension (7%/4%), increased lipase (3%/4%), malignant pleural effusion (1%/4%) and pneumonia (4%/1%).
The oral presentation, "Brigatinib Activity in Patients with ALK+ NSCLC and Intracranial CNS Metastases in Two Clinical Trials," (Abstract #4374, Oral ID OA08.06) will be presented today, Monday, December 5, 2016 in the Schubert 1 Auditorium at 11:57 am ET/16:57 GMT.

Investor and Analyst Briefing and Webcast

Timothy P. Clackson, Ph.D., president of research and development and chief scientific officer of ARIAD will host an investor and analyst briefing on Wednesday, December 7 at 4:00 p.m. Central European Time (10:00 a.m. Eastern Time) to discuss the data presented at WCLC. Dr. Clackson will be joined by Karen Reckamp, M.D., associate professor in the Department of Medical Oncology & Therapeutics Research and co-director of the Lung Cancer and Thoracic Oncology Program at City of Hope Comprehensive Cancer Center (COHCCC).

The live webcast can be accessed by visiting the investor relations section of the Company’s website at View Source The call can be accessed by dialing 844-249-9386 (domestic) or 270-823-1534 (international) five minutes prior to the start time and providing the pass code 20888507. A replay of the call will be available on the ARIAD website approximately two hours after completion of the call and will be archived for three weeks.

About Brigatinib

Brigatinib is an investigational, targeted cancer medicine discovered internally at ARIAD. Brigatinib received Breakthrough Therapy designation from the FDA for the treatment of patients with ALK+ NSCLC whose tumors are resistant to crizotinib, and was granted orphan drug designation by the FDA for the treatment of ALK+ NSCLC. The FDA has accepted brigatinib’s New Drug Application based on data from an earlier datacut, and has granted ARIAD’s request for Priority Review. The FDA has set an action date of April 29, 2017 under the Prescription Drug User Fee Act (PDUFA). ARIAD intends to submit a Marketing Authorization Application (MAA) for brigatinib to the European Medicines Agency (EMA) in early 2017, based on this datacut.

ARIAD has also initiated the Phase 3 ALTA 1L trial to assess the efficacy and safety of brigatinib in comparison to crizotinib in patients with locally advanced or metastatic ALK+ NSCLC who have not received prior treatment with an ALK inhibitor. More information on brigatinib clinical trials, as well as the expanded access program (EAP) for ALK+ NSCLC can be found here.

On December 5, 2016 Spectrum Pharmaceuticals (NasdaqGS: SPPI), a biotechnology company with fully integrated commercial and drug development operations with a primary focus in Hematology and Oncology, reported key presentations of clinical and scientific data related to its products at the San Antonio Breast Cancer Symposium (SABCS), being held in San Antonio, Texas, from December 6-10, 2016 (Press release, Spectrum Pharmaceuticals, DEC 5, 2016, View Source [SID1234516921]).

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For more information about the SABCS meeting and for a complete list of abstracts, please refer to the conference website at View Source

The following are key ROLONTISTM (eflapegrastim) related abstracts being presented at the SABCS meeting:

Abstract # Type Title First Author Date/Time
Location: Hall 1
OT1-01-11 Poster
Randomized phase 3 study of a novel, long-acting G-CSF (eflapegrastim) versus pegfilgrastim in the management of chemotherapy-induced neutropenia in early-stage breast cancer patients receiving docetaxel and cyclophosphamide (TC) (ADVANCE study)

Schwartzberg Wednesday, Dec 7
5:00 PM
P5-11-09 Poster
Sustained efficacy of eflapegrastim in breast cancer patients in a phase 2, open-label, dose-ranging study

Vacirca Friday, Dec 9
5:00 PM
P5-11-07 Poster
Pharmacokinetics of eflapegrastim in a phase 2 open-label dose-ranging study in breast cancer patients receiving TC regimen

Vacirca Friday, Dec 9
5:00 PM
P5-11-08 Poster
Immunogenicity of eflapegrastim in a Phase 2 Open-Label Dose-Ranging Study of eflapegrastim in Breast Cancer Patients Receiving TC Regimen

Vacirca Friday, Dec 9
5:00 PM
The following key poziotinib related abstract will be presented at the SABCS meeting:

Abstract # Type Title First Author Date/Time
Location: Hall 1
OT1-02-10 Poster
A phase 2 study of poziotinib in patients with HER2-positive metastatic breast cancer (MBC) who have received prior HER2 regimens for MBC

Lathrop Wednesday, Dec 7
5:00 PM