Minimal Residual Disease Negativity Data, a Measure of Undetectable Disease, Added to VENCLEXTA® (venetoclax tablets) Label

On September 11, 2018 AbbVie (NYSE: ABBV), a research-based global biopharmaceutical company, reported the U.S. Food and Drug Administration (FDA) has expanded the label for VENCLEXTA (venetoclax tablets) in combination with rituximab to include information about patients with previously-treated chronic lymphocytic leukemia (CLL) who achieved minimal residual disease (MRD)-negativity in the Phase 3 MURANO trial (Press release, AbbVie, SEP 11, 2018, View Source [SID1234529436]).

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MRD-negativity occurs when less than one CLL cell per 10,000 lymphocytes can be detected in the blood or bone marrow using sensitive analytical methods.1 More than half (53 percent [103/194]) of patients treated with the VENCLEXTA and rituximab combination achieved MRD-negativity (undetectable disease) after approximately nine months on therapy (three months after the last dose of rituximab), while 12 percent (23/195) of patients treated with the standard chemoimmunotherapy regimen of bendamustine plus rituximab achieved MRD-negativity.2

"With this label expansion for VENCLEXTA, physicians now have additional information on MRD-negativity, which is becoming an increasingly important goal when caring for their previously-treated CLL patients," said Michael Severino, M.D., executive vice president, research and development, and chief scientific officer, AbbVie. "VENCLEXTA plus rituximab is the first chemotherapy-free combination for previously-treated CLL that allows patients the ability to stop treatment after approximately two years. This label expansion is another important milestone in our efforts to advance care for patients with difficult-to-treat blood cancers."

In the MURANO study, the MRD-negativity rate was evaluated in patients who responded to treatment. The rate of MRD-negativity in patients with a complete response or complete response with incomplete marrow recovery (CR/CRi) at nine months on therapy (three months after the last dose of rituximab) was 3 percent (6/194) in the VENCLEXTA plus rituximab arm and 2 percent (3/195) in the bendamustine plus rituximab arm.2

CLL is typically a slow-growing cancer of the bone marrow and blood in which white blood cells called lymphocytes become cancerous and multiply abnormally.3 In the U.S., CLL accounts for more than 20,000 newly diagnosed cases of leukemia each year.3

"CLL is a chronic, life-altering cancer marked by periods of remission and relapse, making it an emotional rollercoaster for patients. Many patients who enter remission worry that the disease will relapse," said Prof. John Seymour, MBBS, Ph.D., lead investigator of the MURANO study and director of clinical haematology at the Peter MacCallum Cancer Centre & Royal Melbourne Hospital in Australia. "The rates of MRD-negativity seen with VENCLEXTA plus rituximab are very encouraging. A goal in treating patients with CLL is to help them achieve the longest remission possible. MRD-negativity provides us with yet another potential tool for evaluating the effectiveness of new therapies."

VENCLEXTA, a first-in-class medicine that selectively binds and inhibits the B-cell lymphoma-2 (BCL-2) protein, has been granted four Breakthrough Therapy Designations (BTDs) from the FDA.4 In June 2018, the FDA approved, under priority review, VENCLEXTA in combination with rituximab for the treatment of patients with CLL or small lymphocytic lymphoma (SLL), with or without 17p deletion, who have received at least one prior therapy.2 The addition of MRD-negativity data in these previously-treated CLL patients represents the second label expansion for VENCLEXTA in 2018.

VENCLEXTA is being developed by AbbVie and Roche. It is jointly commercialized by AbbVie and Genentech, a member of the Roche Group, in the U.S. and by AbbVie outside of the U.S. Together, the companies are committed to BCL-2 research and to studying venetoclax in clinical trials across several blood and other cancers. 5,6,7,8

About the MURANO Study and MRD Results

A total of 389 patients with relapsed or refractory (R/R) CLL who had received at least one prior therapy were enrolled in the international, multicenter, open-label, randomized (1:1) MURANO study (NCT02005471). The study was designed to evaluate the efficacy and safety of VENCLEXTA in combination with rituximab (194 patients) compared with bendamustine in combination with rituximab (195 patients). The median age of patients in the trial was 65 years (range: 22 to 85 years).2

Efficacy in the U.S. was based on progression-free survival (PFS; the time people live without their disease worsening) as assessed by an Independent Review Committee (IRC). Median PFS with VENCLEXTA in combination with rituximab was not reached compared with 18.1 months for bendamustine in combination with rituximab (hazard ratio: 0.19; 95% confidence interval [CI]: 0.13, 0.28; P<0.0001). The median follow-up for PFS was 23.4 months (range: 0 to 37.4+ months). Additional efficacy endpoints included IRC-assessed response rate (defined as overall response rate [ORR], complete response [CR] plus complete response with incomplete marrow recovery [CRi], nodular partial response [nPR], or partial response [PR]), overall survival (OS) and MRD-negativity).2

MRD was evaluated in patients who achieved a PR or better using allele-specific oligonucleotide polymerase chain reaction (ASO-PCR). The definition of negative status was less than one CLL cell per 10,000 lymphocytes. After nine months on therapy (three months after the last dose of rituximab), the MRD-negativity rate in peripheral blood was 53 percent (103/194) in the VENCLEXTA plus rituximab arm and 12 percent (23/195) in the bendamustine plus rituximab arm.2 The MRD-negativity rate in patients with a CR/CRi at this time point was 3 percent (6/194) in the VENCLEXTA plus rituximab arm and 2 percent (3/195) in the bendamustine plus rituximab arm.

The most common adverse reactions (ARs; ≥20 percent) of any grade for VENCLEXTA in combination with rituximab were neutropenia (65 percent), diarrhea (40 percent), upper respiratory tract infection (39 percent), fatigue (22 percent), cough (22 percent) and nausea (21 percent). In the VENCLEXTA plus rituximab arm, discontinuation due to any ARs occurred in 16 percent of patients, dose reduction in 15 percent, and dose interruption in 71 percent. In the bendamustine plus rituximab arm, ARs led to treatment discontinuation in 10 percent of patients, dose reduction in 15 percent, and dose interruption in 40 percent. In the VENCLEXTA in combination with rituximab arm, neutropenia led to dose interruption of VENCLEXTA in 46 percent of patients and discontinuation in 3 percent, and thrombocytopenia led to discontinuation in 3 percent of patients. In the VENCLEXTA in combination with rituximab arm, fatal ARs that occurred in the absence of disease progression and within 30 days of the last VENCLEXTA treatment and/or 90 days of the last rituximab treatment were reported in 2 percent (4/194) of patients. Serious ARs were reported in 46 percent of patients, with the most frequent (≥5 percent) being pneumonia (9 percent).2

About VENCLEXTA (venetoclax tablets) (U.S.)

VENCLEXTA is a first-in-class medicine that selectively binds and inhibits the B-cell lymphoma-2 (BCL-2) protein. In some blood cancers and other cancerous tumors, BCL-2 builds up and prevents cancer cells from undergoing their natural death or self-destruction process, which is called apoptosis. VENCLEXTA targets the BCL-2 protein and works to restore the process of apoptosis.2

VENCLEXTA is being developed by AbbVie and Roche. It is jointly commercialized by AbbVie and Genentech, a member of the Roche Group, in the U.S. and by AbbVie outside of the U.S. Together, the companies are committed to BCL-2 research and to studying venetoclax in clinical trials across several blood and other cancers.

In April 2016, the U.S. FDA first granted accelerated approval of VENCLEXTA for the treatment of patients with CLL with 17p deletion, as detected by an FDA-approved test, who have received at least one prior therapy.9 The FDA approved this indication under accelerated approval based on overall response rate.9 Based on the results of the MURANO study, VENCLEXTA was granted full approval in June 2018 for the treatment of patients with CLL or SLL, with or without 17p deletion, who have received at least one prior therapy in combination with rituximab or as monotherapy.2

Venetoclax is approved in more than 50 countries, including the U.S. AbbVie, in collaboration with Roche, is currently working with regulatory agencies around the world to bring this medicine to additional eligible patients in need.

For more information, visit www.abbvie.com.

What is VENCLEXTA (venetoclax tablets)?
VENCLEXTA is a prescription medicine used to treat people with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) with or without 17p deletion, who have received at least one prior treatment.

It is not known if VENCLEXTA is safe and effective in children.

Important VENCLEXTA (venetoclax tablets) US Safety Information

What is the most important information I should know about VENCLEXTA?

VENCLEXTA can cause serious side effects, including:

Tumor lysis syndrome (TLS). TLS is caused by the fast breakdown of cancer cells. TLS can cause kidney failure, the need for dialysis treatment, and may lead to death. Your health care provider will do tests to check your risk of getting TLS before starting and during treatment with VENCLEXTA to help reduce your risk of TLS. You may also need to receive intravenous (IV) fluids into your vein. Your health care provider will do blood tests in your first 5 weeks of treatment to check you for TLS during treatment with VENCLEXTA. It is important to keep your appointments for blood tests. Tell your health care provider right away if you have any symptoms of TLS during treatment with VENCLEXTA, including fever, chills, nausea, vomiting, confusion, shortness of breath, seizures, irregular heartbeat, dark or cloudy urine, unusual tiredness, or muscle or joint pain.

Drink plenty of water when taking VENCLEXTA to help reduce your risk of getting TLS. Drink 6 to 8 glasses (about 56 ounces total) of water each day, starting 2 days before your first dose, on the day of your first dose of VENCLEXTA, and each time your dose is increased.

Who should not take VENCLEXTA?

Certain medicines must not be taken when you first start taking VENCLEXTA and while your dose is being slowly increased because of the risk of increased tumor lysis syndrome.

Tell your health care provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. VENCLEXTA and other medicines may affect each other, causing serious side effects.
Do not start new medicines during treatment with VENCLEXTA without first talking with your health care provider.
Before taking VENCLEXTA, tell your health care provider about all of your medical conditions, including if you:

Have kidney or liver problems.
Have problems with your body salts or electrolytes, such as potassium, phosphorus, or calcium
Have a history of high uric acid levels in your blood or gout
Are scheduled to receive a vaccine. You should not receive a "live vaccine" before, during or after treatment with VENCLEXTA until your health care provider tells you it is okay. If you are not sure about the type of immunization or vaccine, ask your health care provider. These vaccines may not be safe or may not work as well during treatment with VENCLEXTA.
Are pregnant or plan to become pregnant. VENCLEXTA may harm your unborn baby. If you are able to become pregnant, your health care provider should do a pregnancy test before you start treatment with VENCLEXTA, and you should use effective birth control during treatment and for 30 days after the last dose of VENCLEXTA. If you become pregnant or think you are pregnant, tell your health care provider right away.
Are breastfeeding or plan to breastfeed. It is not known if VENCLEXTA passes into your breast milk. Do not breastfeed during treatment with VENCLEXTA.
What should I avoid while taking VENCLEXTA?
You should not drink grapefruit juice, eat grapefruit, Seville oranges (often used in marmalades), or starfruit while you are taking VENCLEXTA. These products may increase the amount of VENCLEXTA in your blood.

What are the possible side effects of VENCLEXTA?

VENCLEXTA can cause serious side effects, including:

Low white blood cell count (neutropenia). Low white blood cell counts are common with VENCLEXTA, but can also be severe. Your health care provider will do blood tests to check your blood counts during treatment with VENCLEXTA. Tell your health care provider right away if you have a fever or any signs of an infection while taking VENCLEXTA.
The most common side effects of VENCLEXTA when used in combination with rituximab include low white blood cell count, diarrhea, upper respiratory tract infection, cough, tiredness, and nausea.

The most common side effects of VENCLEXTA when used alone include low white blood cell count, diarrhea, nausea, upper respiratory tract infection, low red blood cell count, tiredness, low platelet count, muscle and joint pain, swelling of your arms, legs, hands, and feet, and cough.

VENCLEXTA may cause fertility problems in males. This may affect your ability to father a child. Talk to your health care provider if you have concerns about fertility.

These are not all the possible side effects of VENCLEXTA. Tell your health care provider if you have any side effect that bothers you or that does not go away.

People are encouraged to report negative side effects of prescription drugs to the FDA. Visit www.fda.gov/medwatch or call 1-800-FDA-1088.

Daiichi Sankyo’s FLT3 Inhibitor Quizartinib Receives Orphan Drug Designation from Japanese MHLW for FLT3-Mutated AML

On September 11, 2018 Daiichi Sankyo Company, Limited (hereafter, Daiichi Sankyo) reported that quizartinib, an investigational FLT3 inhibitor, has been granted Orphan Drug designation by the Japan Ministry of Health, Labour and Welfare (MHLW) for the treatment of FLT3-mutated acute myeloid leukemia (AML) (Press release, Daiichi Sankyo, SEP 11, 2018, View Source [SID1234529382]).

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"There is a critical need for new treatment options for patients with FLT3-ITD AML, especially given the poor prognosis associated with this subtype of AML," said Koichi Akahane, PhD, MBA, Executive Officer, Head of Oncology Function, R&D Division, Daiichi Sankyo. "Following the recent U.S. FDA Breakthrough Therapy designation for quizartinib, receiving Orphan Drug designation is another important regulatory milestone that will help accelerate the development of quizartinib in Japan. We look forward to working closely with the Japan MHLW to bring quizartinib to patients as quickly as possible."

The Japan MHLW Orphan Drug designation system is designed to promote research activities and support the development of orphan drugs for serious, difficult-to-treat diseases that affect fewer than 50,000 patients in Japan, and for which significant unmet medical need exists. An investigational compound can qualify for Orphan Drug designation if there is no approved alternative treatment option or if high efficacy or safety compared to existing treatment options is expected. Compounds receiving Orphan Drug designation qualify for several measures intended to support development, including, but not limited to, guidance and subsidies for research and development activities, priority consultation for clinical development and priority review of applications.

Quizartinib is the first FLT3 inhibitor to prolong overall survival as an oral, single agent compared to chemotherapy in a randomized, phase 3 trial (QuANTUM-R) in patients with relapsed/refractory FLT3-ITD

AML. Results of QuANTUM-R were presented during the plenary program at the 23rd Congress of the

European Hematology Association in June 2018.

The safety profile observed in QuANTUM-R appears consistent with that observed at similar doses in the quizartinib clinical development program. Incidence of treatment-emergent adverse events was comparable between patients who received single agent quizartinib and those who received salvage chemotherapy. The most common adverse events (>30 percent, any Grade) in patients treated with quizartinib included nausea, thrombocytopenia, fatigue, musculoskeletal pain, pyrexia, anemia, neutropenia, febrile neutropenia, vomiting and hypokalemia.

About Quizartinib

Quizartinib, the lead investigational agent in the AML Franchise of the Daiichi Sankyo Cancer Enterprise, is an oral selective FLT3 inhibitor currently in phase 3 development for relapsed/refractory FLT3-ITD AML (QuANTUM-R) in the U.S. and EU and newly-diagnosed FLT3-ITD AML (QuANTUM-First) in the U.S., EU and Japan; and phase 2 development for relapsed/refractory FLT3-ITD AML in Japan.

In addition to Orphan Drug designation in Japan, quizartinib has been granted Breakthrough Therapy designation for the treatment of adult patients with relapsed/refractory FLT3-ITD AML and Fast Track designation for the treatment of relapsed/refractory AML by the U.S. Food and Drug Administration (FDA). Quizartinib also has received Orphan Drug designation by both the FDA and the European Medicines Agency (EMA) for the treatment of AML. Quizartinib is an investigational agent that has not been approved for any indication in any country. Safety and efficacy have not been established.

About FLT3-ITD Acute Myeloid Leukemia
AML is an aggressive blood and bone marrow cancer that causes uncontrolled growth and accumulation of malignant white blood cells that fail to function normally and interfere with the production of normal blood cells.1 FLT3 gene mutations are one of the most common genetic abnormalities in AML.2 FLT3-ITD is the most common FLT3 mutation, affecting approximately one in four patients with AML.3,4,5,6 Patients with FLT3-ITD AML have a worse overall prognosis, including an increased incidence of relapse, an increased risk of death following relapse, and a higher likelihood of relapse following hematopoietic stem cell transplantation as compared to those without this mutation.7,8

Incyte and Foundation Medicine Announce Agreement to Develop Companion Diagnostic for Pemigatinib (INCB54828), a Selective FGFR Inhibitor, in Patients with Cholangiocarcinoma

On September 11, 2018 Incyte Corporation (NASDAQ:INCY) and Foundation Medicine, Inc., reported that the companies have entered into an agreement for the development, regulatory support and commercialization of companion diagnostics (CDx), with an initial focus on CDx development for pemigatinib (INCB54828), Incyte’s selective FGFR1/2/3 inhibitor, in patients with cholangiocarcinoma (Press release, Incyte, SEP 11, 2018, View Source [SID1234529610]). The initial CDx, which will include detection of activating FGFR2 translocations, is expected to be incorporated into FoundationOneCDx, Foundation Medicine’s FDA-approved comprehensive genomic profiling (CGP) assay and broad CDx platform.

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"There is an urgent need for a novel, biomarker-based, targeted therapeutic approach for patients with cholangiocarcinoma. The initial goal of this collaboration is to develop a companion diagnostic to enable testing at diagnosis of stage IV disease, with the aim of helping to reduce morbidity and mortality, and we are very pleased to be working with Foundation Medicine as we seek to improve outcomes for these patients," said Steven Stein, M.D., Chief Medical Officer, Incyte. "Incyte is evaluating pemigatinib in patients with cholangiocarcinoma as part of the FIGHT clinical development program; initial data have been accepted for presentation at the European Society of Medical Oncology (ESMO) (Free ESMO Whitepaper) meeting in Munich this October."

"We’re committed to helping our biopharma partners bring biomarker-driven therapies to cancer patients. Partnerships with innovative biopharma companies, such as Incyte, who leverage our FDA-approved platform to help accelerate companion diagnostics development, are essential to achieving this mission," said Melanie Nallicheri, Chief Business Officer and Head of Biopharma at Foundation Medicine. "We’re proud to partner with Incyte to advance development of a potential new precision oncology treatment option for cholangiocarcinoma."

About FGFR and Pemigatinib (INCB54828)

Fibroblast growth factor receptors (FGFRs) play an important role in tumor cell proliferation and survival, migration and angiogenesis (the formation of new blood vessels). Activating mutations, translocations and gene amplifications in FGFRs are closely correlated with the development of various cancers.

Pemigatinib is a potent, selective, oral inhibitor of FGFR isoforms 1, 2 and 3 which, in preclinical studies, has demonstrated selective pharmacologic activity against cancer cells with FGFR alterations. Phase 2 studies investigating the safety and efficacy of pemigatinib monotherapy across several FGFR-driven malignancies are ongoing—the FIGHT (FIbroblast Growth factor receptor in oncology and Hematology Trials) clinical trial program currently comprises FIGHT-201 in patients with metastatic or surgically unresectable bladder cancer, including with activating FGFR3 alterations; FIGHT-202 in patients with metastatic or surgically unresectable cholangiocarcinoma who have failed previous therapy, including with activating FGFR2 translocations; and FIGHT-203 in patients with myeloproliferative neoplasms with activating FGFR1 translocations.

Editas Medicine Announces U.S. Court of Appeals for the Federal Circuit Affirms Favorable U.S. Patent and Trademark Office Decision in CRISPR Interference

On September 10, 2018 Editas Medicine, Inc. (NASDAQ: EDIT), a leading genome editing company, reported that the U.S. Court of Appeals for the Federal Circuit (CAFC) affirmed the U.S. Patent and Trademark Office (USPTO) decision that ended the U.S. patent interference between the University of California, the University of Vienna, and Emmanuelle Charpentier (collectively, UC) and the Broad Institute, Inc. (Broad) concerning certain CRISPR/Cas9 patents Editas Medicine exclusively licenses from Broad (Press release, Editas Medicine, SEP 10, 2018, View Source;p=RssLanding&cat=news&id=2366755 [SID1234529383]). This favorable action by the CAFC upholds the USPTO decision issued in February 2017, granting Broad’s motion for no interference-in-fact.

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"We are pleased with the Federal Circuit’s decision affirming the Patent Trial and Appeal Board decision on the patents that were granted to the Broad Institute for its innovative and fundamental work on CRISPR/Cas9 genome editing," said Katrine Bosley, President and Chief Executive Officer, Editas Medicine. "This decision is highly favorable for Editas and for the Broad as it reaffirms the strength of our intellectual property foundation and has profound implications for making CRISPR medicines."

Editas Medicine’s foundational intellectual property includes issued patents covering fundamental aspects of both CRISPR/Cas9 and CRISPR/Cpf1 (also known as CRISPR/Cas12a) gene editing. The patents broadly cover CRISPR/Cas9 and CRISPR/Cpf1 gene editing in eukaryotic cells, which includes all human cells. Successfully editing this cell type is essential to making CRISPR-based medicines. Overall, the Company holds a wide range of fundamental intellectual property directed to all of the components of its genome editing platform as well as product-enabling and product-specific intellectual property.

In 2014, the USPTO granted the first of several foundational patents to Broad with broad claims covering CRISPR/Cas9 in eukaryotic cells. In 2016, the USPTO declared an interference proceeding between Broad and UC that involved several of Broad’s issued CRISPR patents. While scientists in both groups had made important scientific contributions to the field, this proceeding was initiated by the USPTO to determine which of the two groups first invented the use of CRISPR/Cas9 for editing DNA in eukaryotic cells.

In February 2017, the Patent Trial and Appeal Board of the USPTO determined that the patent claims that had been granted to Broad were separately patentable from, and thus, do not interfere with, the claims of the UC application. This ruling ended the interference proceeding and upheld Broad’s fundamental CRISPR/Cas9 patents as originally granted. Today’s decision affirms that USPTO decision from February 2017. The Broad patents continue to be valid and in force. Foundational claims covering the use of CRISPR/Cas9 for gene editing in eukaryotic cells have also issued to Broad as patents in each of the United States, Europe, and Australia.

CCAB And Triumvira Immunologics Announce Triumvira’s License Agreement with University of Toronto for the Discovery of Antibody Drug Development Candidates

On September 10, 2018 The Centre for the Commercialization of Antibodies and Biologics (CCAB) and Triumvira Immunologics, Inc. (Triumvira), reported a new licensing agreement between the University of Toronto (U of T) and Triumvira (Press release, Triumvira Immunologics, SEP 10, 2018, View Source [SID1234529369]). The agreement provides Triumvira with an exclusive license for antibodies discovered at the U of T on specified therapeutic targets. Triumvira is a privately held biopharmaceutical company with R&D facilities in Hamilton, ON, that is developing a novel platform for engineering T cells to attack multiple cancer types.

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CCAB is the assigned agent for the U of T for the commercialization of a large portfolio of human antibodies. Under the terms of the agreement, U of T will receive up-front fees, milestone payments and royalty payments on net sales of products on three therapeutic targets: BCMA, ROR1 and one undisclosed target.

"We are very pleased to be working with The Centre for the Commercialization of Antibodies and Biologics and the University of Toronto under this new licencing agreement," said Paul Lammers, MD, MSc, President and Chief Executive Officer of Triumvira. "This partnership is critical as we work to bring new treatments to patients in need through our proprietary T Cell-Antigen Coupler (TAC) technology."

Triumvira’s lead therapeutic candidate, TAC01-CD19, is a CD19-directed T cell product for the treatment of B cell malignancies and is anticipated to enter Phase I clinical trials in H1 2019 in patients with diffuse large B cell lymphoma (DLBCL). The company is also developing a series of products for solid tumors.

"Collaboration is a vital part in the development of new therapeutics. These types of agreements continue to strengthen the connection between academia and industry and help to translate the wealth of scientific knowledge from the laboratories at our world-class universities to the clinic," CCAB Chief Executive Officer Robert Verhagen said.