On May 24, 2016 a wholly-owned subsidiary of Spectrum Pharmaceuticals, Inc. ("Spectrum"), Allos Therapeutics Inc. (the "Company"), and Teva Pharmaceuticals USA, Inc. ("Teva"), reported that it has entered into a settlement agreement to resolve their patent litigation relating to Folotyn (pralatrexate injection) (Filing, 8-K, Spectrum Pharmaceuticals, MAY 25, 2016, View Source [SID:1234512774]).

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As a result of the settlement, Teva will be permitted to market a generic version of Folotyn in the United States on December 1, 2022 or earlier under certain circumstances. Details of the settlement are confidential, and the parties will submit the agreement to the Federal Trade Commission and the Department of Justice. The parties will request that the court enter an order, in which it will dismiss the Company’s litigation against Teva. The Company’s litigation against other generic filers continues. This litigation is described in further detail in Part II, Item 1 of Spectrum’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2016, filed with the U.S. Securities and Exchange Commission on May 6, 2016.

On May 25, 2016 Seattle Genetics, Inc. (NASDAQ: SGEN) reported initiation of a pivotal phase 3 clinical trial, called CASCADE, evaluating vadastuximab talirine (SGN-CD33A; 33A) in combination with azacitidine (Vidaza) or decitabine (Dacogen) in older patients with newly diagnosed acute myeloid leukemia (AML) (Press release, Seattle Genetics, MAY 25, 2016, View Source [SID:1234512772]).

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33A is an antibody-drug conjugate (ADC) targeted to CD33 utilizing Seattle Genetics’ newest technology, comprising an engineered cysteine antibody (EC-mAb) stably linked to a highly potent DNA binding agent called a pyrrolobenzodiazepine (PBD) dimer. CD33 is expressed on leukemic blasts in nearly all AML patients and expression is generally consistent regardless of age, cytogenetic abnormalities or underlying mutations. Azacitidine and decitabine are hypomethylating agents (HMAs) commonly used in the treatment of older AML patients.

"Acute myeloid leukemia, or AML, is a devastating disease representing a significant unmet medical need. It impacts approximately 20,000 people in the U.S. each year, with few effective treatment options. Older AML patients have a particularly poor prognosis as the majority have high risk disease characteristics and a median survival of ten months or less with available therapies," said Clay Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. "We have a robust development strategy, with several ongoing clinical trials across multiple lines of therapy in myeloid malignancies to explore 33A as a treatment option broadly in AML. This pivotal phase 3 CASCADE trial is a significant corporate milestone and an important step in our goal to improve outcomes for AML patients."

The phase 3 CASCADE study is a randomized, double-blind, placebo-controlled, global clinical trial. It is designed to evaluate if 33A in combination with azacitidine or decitabine can extend overall survival compared to azacitidine or decitabine alone in older patients with newly diagnosed AML. Patients will be randomized on a 1:1 ratio to be treated with an HMA plus 33A or an HMA plus placebo. The secondary endpoints include the comparison of composite complete remission rate (complete remission and complete remission with incomplete hematologic recovery; CR/CRi), event-free and leukemia-free survival, duration of response, safety, and 30- and 60-day mortality rates. The phase 3 trial will enroll approximately 500 patients globally. For more information about the trial, including enrolling centers, please visit www.clinicaltrials.gov.

Interim results from the ongoing phase 1 study evaluating 33A in combination with HMAs in frontline AML and as monotherapy in primarily relapsed AML were presented at the 2015 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition. Data from the phase 1 33A combination trial demonstrated that 15 of 23 (65 percent) evaluable patients achieved CR/CRi. At a median follow-up of 7.7 months, median survival had not yet been reached, and 72 percent of patients remained alive and on study.

Updated data from the ongoing phase 1 study of 33A in combination with HMAs will be presented in an oral presentation at the 2016 European Hematology Association (EHA) (Free EHA Whitepaper) Congress taking place June 9 – 12, 2016, in Copenhagen, Denmark.

In addition to the phase 3 CASCADE trial, Seattle Genetics is evaluating 33A broadly across multiple lines of therapy in patients with AML and myelodysplastic syndromes (MDS), including the following ongoing trials:

A phase 1 trial of 33A monotherapy and in combination with HMAs in AML patients who have relapsed/declined intensive frontline therapy or are newly diagnosed;
A phase 1b trial in combination with standard-of-care intensive chemotherapy (7+3), consisting of cytarabine and daunorubicin, for younger fit patients with AML;
A phase 1/2 trial in patients with relapsed or refractory AML evaluating 33A monotherapy as a pre-conditioning regimen prior to an allogeneic stem cell transplant and also for use as maintenance therapy following transplant; and,
A phase 1/2 trial of 33A in combination with azacitidine in patients with previously untreated MDS.
More information about SGN-CD33A and ongoing clinical trials can be found at www.ADC-CD33.com.

With more than 15 years of experience and innovation, Seattle Genetics is the leader in developing ADCs. ADCs are monoclonal antibodies that are designed to selectively deliver cell-killing agents to tumor cells. This approach is intended to spare non-targeted cells and, thus, reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity.

About Acute Myeloid Leukemia

Acute myeloid leukemia, also called acute myelocytic leukemia or AML, is an aggressive type of cancer of the bone marrow and blood that progresses rapidly without treatment. AML is a cancer that starts in the cells that are supposed to mature into different types of blood cells. AML starts in the bone marrow (the interior part of bones, where new blood cells are made) and quickly moves into the blood. According to the American Cancer Society, in 2016 approximately 20,000 new cases of AML (mostly in adults) will be diagnosed and nearly 10,500 deaths will occur from AML (almost all will be in adults).

About Vadastuximab Talirine (SGN-CD33A)

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

On May 25, 2016 DelMar Pharmaceuticals, Inc. (OTCQX: DMPID) ("DelMar" and the "Company"), a company focused on developing and commercializing proven cancer therapies in new orphan drug indications, reported the successful completion of an End of Phase 2 meeting with the U.S. Food and Drug Administration (FDA) (Press release, DelMar Pharmaceuticals, MAY 25, 2016, View Source [SID:1234512771]).

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"Our End-of-Phase 2 meeting was an important milestone for the Company as we advance the clinical development of VAL-083," stated Jeffrey Bacha, chairman and CEO of DelMar Pharmaceuticals. "We are pleased with the FDA’s guidance on our Phase 3 trial design in patients with glioblastoma who have failed prior therapy with temozolomide and bevacizumab (Avastin), and we look forward to finalizing the trial design and initiating the study as quickly as possible."

DelMar’s advanced development program will feature a single randomized Phase 3 study measuring survival outcomes compared to a "physicians’ choice" control, which, if successful, would serve as the basis for a New Drug Application (NDA) submission for VAL-083. The control arm will consist of a limited number of salvage chemotherapies currently utilized in the treatment of Avastin-failed GBM. The final pivotal trial design will be confirmed with the FDA following further discussions with the Company’s clinical advisors.

The FDA confirmed that it will consider the totality of data available, including data obtained from DelMar’s other planned clinical trials in related GBM populations, when assessing the NDA. The FDA also noted that DelMar can rely on prior US National Cancer Institutes (NCI) studies and historical literature to support non-clinical data required for an NDA filing and that DelMar will have the option to file under a 505(b)(2) strategy, which allows a sponsor to rely on already established safety and efficacy data in support an NDA.

"There is a major unmet medical need in refractory glioblastoma," said Mr. Bacha. "The encouraging data from our clinical trials to date, combined with historical data from prior clinical trials from the NCI, suggest that VAL-083 has the potential to improve therapeutic outcomes for GBM patients who currently have no viable treatment options. We are now one step closer to achieving that goal."

About VAL-083

VAL-083 is a "first-in-class," small-molecule chemotherapeutic. In more than 40 Phase I and II clinical studies sponsored by the U.S. National Cancer Institute, VAL-083 demonstrated clinical activity against a range of cancers including lung, brain, cervical, ovarian tumors and leukemia both as a single-agent and in combination with other treatments. VAL-083 is approved in China for the treatment of chronic myelogenous leukemia (CML) and lung cancer, and has received orphan drug designation in Europe and the U.S. for the treatment of malignant gliomas. DelMar recently announced that the USFDA’s Office of Orphan Products had also granted an orphan designation to VAL-083 for the treatment of medulloblastoma.

DelMar has demonstrated that VAL-083’s anti-tumor activity is unaffected by the expression of MGMT, a DNA repair enzyme that is implicated in chemotherapy resistance and poor outcomes in GBM patients following standard front-line treatment with Temodar (temozolomide).

DelMar conducted a Phase I/II clinical trial in GBM patients whose tumors have progressed following standard treatment with temozolomide, radiotherapy, bevacizumab and a range of salvage therapies. Patients were enrolled at five clinical centers in the United States: Mayo Clinic (Rochester, MN); UCSF (San Francisco, CA) and three centers associated with the Sarah Cannon Cancer Research Institute (Nashville, TN, Sarasota, FL and Denver, CO) (clinicaltrials.gov identifier: NCT01478178). DelMar announced the completion of enrollment in a Phase II expansion cohort in September, 2015.

About Glioblastoma Multiforme (GBM)

Glioblastoma multiforme (GBM) is the most common and most malignant form of brain cancer. Approximately 15,000 people are diagnosed with GBM each year in the U.S., with similar incidence in Europe. Standard of care is surgery, followed by either radiation therapy, or radiation therapy combined with temozolomide. Approximately 60 percent of GBM patients treated with temozolomide experience tumor progression within one year. More than half of glioblastoma patients will fail the currently approved therapies and face a very poor prognosis.

On May 25, 2016 Alkermes plc (NASDAQ: ALKS) reported the initiation of a phase 1 clinical study of the company’s immuno-oncology drug candidate, ALKS 4230 (formerly referred to as RDB 1450), a novel Selective Effector Cell Activator (SECA) protein designed for targeted interleukin-2 (IL-2) receptor activation (Press release, Alkermes, MAY 25, 2016, View Source [SID:1234512770]).

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The multi-center phase 1 study is designed to evaluate the safety, tolerability and immunological-pharmacodynamic effects of ALKS 4230 in the treatment of patients with solid tumors.

The phase 1 study will be conducted in two stages: a dose-escalation stage followed by a dose-expansion stage. In the first stage of the study, ALKS 4230 will be administered as an intermittent intravenous infusion with ascending doses in patients with solid tumors who are refractory or intolerant to established therapies. This first stage of the study is designed to determine a maximum tolerated dose, and to identify the optimal dose range of ALKS 4230 based on measures of immunological-pharmacodynamic effects. Following the identification of the optimal dose range of ALKS 4230 in the first stage of the study, the dose-expansion stage of the study will evaluate ALKS 4230 in patients with selected solid tumor types. Initial results from the first stage of the phase 1 study are expected in 2017.

"ALKS 4230 is a unique immuno-oncology candidate that is designed to harness the IL-2 mechanism in a selective way that enhances tumor-killing immune cells, so that a patient’s own immune system can be activated in order to fight cancer more effectively," said Elliot Ehrich, M.D., Chief Medical Officer of Alkermes. "We have designed this initial clinical study of ALKS 4230 to be highly informative and to position us for phase 2 studies, including those that may include ALKS 4230 in combination with other immuno-oncology therapies. We are excited about the start of the clinical program and the potential for ALKS 4230 to make an impact for patients with cancer."

About ALKS 4230 and the SECA Immuno-Oncology Program
ALKS 4230 is a novel selective effector cell activator (SECA) protein designed to preferentially bind and signal through the intermediate affinity interleukin-2 (IL-2) receptor complex, thereby selectively activating and increasing the number of immunostimulatory tumor-killing immune cells while avoiding the expansion of immunosuppressive cells that interfere with anti-tumor response. The selectivity of ALKS 4230 is designed to leverage the proven anti-tumor effects while overcoming limitations of existing IL-2 therapy which activates both immunostimulatory and immunosuppressive receptors.

SECA proteins are engineered using Alkermes’ proprietary PICASSOTM circular permutation technology leveraging human protein biology to achieve their unique mechanism of action.