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Glioblastoma multiforme (GBM) is the most common brain and central nervous system (CNS) cancer, accounting for 15.1% of all primary brain tumors, and 55.1% of all gliomas. There are an estimated 12,120 new glioblastoma cases predicted in 2016 in the U.S. Malignant brain tumors are the most common cause of cancer-related deaths in adolescents and young adults aged 15-39 and the most common cancer occurring among 15-19 year olds in the U.S. While GBM is a rare disease (2-3 cases per 100,000 person life years in U.S. and E.U.), it is quite lethal with 5-year survival rates historically less than 10%. Chemotherapy with temozolomide and radiation are shown to extend mean overall survival from 4.5 to 15 months, while surgery remains the standard of care. GBM remains difficult to treat due to the inherent resistance of the tumor to conventional therapies.

Immunotherapy approaches targeting brain tumors offer promise over conventional treatments. IL13Rα2 is an attractive target for CAR-T therapy as it has limited expression in normal tissue but is over-expressed on the surface of greater than 50% of GBM’s. CAR-T cells are designed to express membrane-tethered IL-13 receptor ligand (IL-13) with high affinity for IL13Rα2 and reduced binding to IL13Rα1 in order to reduce healthy tissue targeting.

We are developing an optimized CAR-T product incorporating enhancements in CAR design and T-cell engineering to improve antitumor potency and T-cell persistence. We include a second generation hinge optimized CAR containing mutations in the IgG4 linker to reduce off target Fc interactions as well as the 41BB (CD137) co-stimulatory signaling domain for improved survival and maintenance of memory T-cells as well as extracellular domain of CD20 as a selection/safety marker. In order to further improve persistence, central memory T-cells (TCM) are isolated and enriched. The manufacturing process limits ex vivo expansion in order to reduce T-cell exhaustion and maintain a TCM phenotype.

In collaboration with the COH, we have an on-going phase I clinical study to assess the feasibility and safety of using TCM enriched IL13Rα2-specific CAR engineered T-cells and are currently treating patients with recurrent/refractory GBM. We will assess the T-cell persistence and determine the potential immunogenicity of the cells to determine a recommended phase II dose.

On April 18, 2016 Innate Pharma SA (the "Company" – Euronext Paris: FR0010331421 – IPH) reported data on a research program to develop a CD73 checkpoint inhibitor antibody in oncology at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2016 in New Orleans, Louisiana, USA (Press release, Innate Pharma, APR 18, 2016, View Source [SID:1234511075]). This new anti-CD73 project complements Innate’s first-in-class anti-CD39 program strengthening the Company’s positioning in targeting the tumor microenvironment.

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CD73 and CD39 are two enzymes which play a major role in promoting immunosuppression through the pathway degrading adenosine triphosphate (ATP) into adenosine. CD73 is active on the last step of the degradation pathway, where it is the enzyme that actually degrades AMP* into adenosine.

Poster #2344 presented a panel of newly generated antibodies that block CD73 function. They all bind with high affinity and specificity to the CD73 enzyme, but to distinct epitopes and display different mechanisms of inhibition, including direct blocking of CD73 enzymatic activity or down-modulation of CD73 membrane expression. All antibodies strongly reduce AMP catabolism and efficiently reverse adenosine-mediated T cell suppression in vitro. The antibodies displaying the most interesting features were humanized and further evaluation of their activity is ongoing.

Nicolai Wagtmann, CSO of Innate Pharma, said: "This program adds to our innovative and diversified portfolio of checkpoint inhibitors. We are entering the very exciting and novel area of microenvironment checkpoint inhibition which complements other immuno-oncology approaches. Our anti-CD73 and anti-CD39 antibodies each have potential as single-agent therapeutics and for combination with other checkpoint blockers notably targeting T or NK cells".

On April 18, 2016 Sangamo BioSciences, Inc. (NASDAQ: SGMO), the leader in therapeutic genome editing, reported that data from several ZFP Therapeutic programs will be presented at the 19th Annual Meeting of the American Society of Gene & Cell Therapy (ASGCT) (Free ASGCT Whitepaper) to be held in Washington, D.C. from May 4-7, 2016 (Press release, Sangamo BioSciences, APR 18, 2016, View Source [SID:1234511044]).

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Sangamo BioSciences, Inc. (PRNewsFoto/Sangamo BioSciences, Inc.)
Eight oral and seven poster presentations will be given by Sangamo scientists and their academic collaborators. These presentations will detail data from Sangamo’s therapeutic and research programs and will focus on lysosomal storage disorders and other monogenic diseases, hemoglobinopathies, HIV/AIDS, cancer immunotherapy and advancements in technology, including improvements in modification efficiency. In addition, Sangamo scientists have been invited to present in two scientific symposia focused on clinical applications of genome editing and gene and cell therapeutics targeting the liver.

"The data to be presented at this year’s ASGCT (Free ASGCT Whitepaper) Annual Meeting from our therapeutic and research programs cover a wide range of applications and demonstrate the versatility of our zinc finger nuclease genome editing platform and the expertise of our research and development teams," said Edward Lanphier, Sangamo’s president and chief executive officer. "Sangamo continues to lead the clinical development of therapeutic genome editing and ASGCT (Free ASGCT Whitepaper) offers an opportunity for us to present the broad capabilities of our highly leverageable technology platform in multiple therapeutic areas."

The following presentations are scheduled at the ASGCT (Free ASGCT Whitepaper) Meeting sessions:

Invited Presentations at Scientific Symposia

Genome Editing in Primary Human Cells and Organs: Toward the Goal of Engineering Genetic Cures – Michael C. Holmes, Ph.D., Sangamo BioSciences
Special Symposium on Concepts and Clinical Applications of Genome Editing
Invited Talk – Wednesday, May 4, 2016

ZFN-Mediated Genome Editing in the Liver – Towards Correcting Hemophilias and Lysosomal Storage Diseases – Thomas Wechsler, Ph.D., Sangamo BioSciences
Scientific Symposium: Targeting the Liver with Gene and Cell Therapeutics
Invited Talk – Wednesday, May 4, 2016

Lysosomal Storage Disorders

In Vivo Zinc-Finger Nuclease Mediated Iduronate-2-Sulfatase (IDS) Target Gene Insertion and Correction of Metabolic Disease in a Mouse Model of Mucopolysaccharidosis Type II (MPS II) – Abstract #484
Session: Targeted Genome Editing: In Vivo Genome Editing
Oral Presentation – Friday, May 6, 2016

ZFN-Mediated Liver-Targeting Gene Therapy Corrects Systemic and Neurological Disease of Mucopolysaccharidosis Type I – Abstract #485
Session: Targeted Genome Editing: In Vivo Genome Editing
Oral Presentation – Friday, May 6, 2016
HIV/AIDS

CCR5 Gene Edited Hematopoietic Stem Cells Engraft in Diverse Anatomical Locales and Undergo SHIV-Dependent Positive Selection in Nonhuman Primates – Abstract #38
Session: Targeted Genome Editing: Gene Editing in Hematopoietic Cells
Oral Presentation – Wednesday, May 4, 2016

In Vivo Inhibition of HIV-1 in NSG Mice After Transduction of Primary Human T Cells with CXCR4 Conjugated to an HR2 Peptide – Abstract #427
Session: Immunological Aspects of Gene Therapy I
Poster Presentation – Thursday, May 5, 2016

Pre-Clinical Development and Qualification of ZFN-Mediated Disruption of CCR5 Gene Sequences in Human Hematopoietic Stem and Progenitor Cells – Abstract #734
Session: Targeted Genome Editing: Methods and Technology
Oral Presentation – Saturday, May 7, 2016
Hemoglobinopathies

Targeted Gene Addition in CD34+ Cells from Healthy Donors and Fanconi Anemia Patients – Abstract #558
Session: Targeted Genome Editing III
Poster Presentation – Friday, May 6, 2016
Cancer Immunotherapy

Single Chain TCR Gene Editing in Adoptive Cell Therapy for Multiple Myeloma – Abstract #752
Session: Cancer-Immunotherapy, Cancer Vaccines III
Oral Presentation – Saturday, May 7, 2016
Monogenic Diseases

Towards Clinical Translation of Hematopoietic Stem Cell Gene Editing for the Correction of SCID-X1 Mutations – Abstract #37
Session: Targeted Genome Editing: Gene Editing in Hematopoietic Cells
Oral Presentation – Wednesday, May 4, 2016

Correction of SCID-X1 by Targeted Genome Editing of Hematopoietic Stem/Progenitor Cells (HSPC) in the Mouse Model – Abstract #42
Session: Targeted Genome Editing: Gene Editing in Hematopoietic Cells
Oral Presentation – Wednesday, May 4, 2016

Technology Developments and other Applications

Highly Efficient Homology-Driven Genome Editing in Human T Cells with Combined Zinc-Finger Nuclease mRNA and AAV6 Donor Delivery and Improved Efficiency Under Serum-Free Conditions – Abstract #133
Session: Targeted Genome Editing I
Poster Presentation – Wednesday, May 4, 2016

Valproic Acid Treatment Enhances Hematopoietic Stem and Progenitor Cell Multipotency Ex Vivo for Enhanced Long-Term Engraftment of Gene-Modified Cells – Abstract #432
Session: Immunological Aspects of Gene Therapy I
Poster Presentation – Thursday, May 5, 2016

Highly Efficient, ZFN-Driven Knockout of Surface Expression of the T-Cell Receptor and HLA Class I Proteins in Human T-Cells for Enhancing Allogeneic Adoptive Cell Therapies – Abstract #641
Session: Cancer-Immunotherapy, Cancer Vaccines III
Poster Presentation – Friday, May 6, 2016

Enhanced FVIII AAV Vector Cassette Produces Improved Virus Yields and Supraphysiological FVIII Levels In Vivo – Abstract #684
Session: Hematologic & Immunologic Diseases II
Poster Presentation – Friday, May 6, 2016

Genome Editing of Inducible Cell Lines for Scalable Production of Improved Lentiviral Vectors for Human Gene Therapy – Abstract #286
Session: Vector and Cell Engineering/Manufacturing
Oral Presentation – Thursday, May 5, 2016

Characterization of Chromosomal Alterations Using a Zinc-Finger Nuclease Targeting Both the Beta- and Delta-Globin Gene Loci in Hematopoietic Stem/Progenitor cells – Abstract #118
Session: Targeted Genome Editing I
Poster Presentation – Wednesday, May 4, 2016

All abstracts for the ASGCT (Free ASGCT Whitepaper) meeting are available online at 2016 ASGCT (Free ASGCT Whitepaper) Annual Meeting Abstracts.

On April 18, 2016 Genzyme, the specialty care global business unit of Sanofi, reported that positive new brain volume data from an ongoing clinical study of Lemtrada (alemtuzumab) will be presented at the 68th American Academy of Neurology (AAN) Annual Meeting (Press release, Genzyme, APR 18, 2016, View Source [SID:1234511027]). In addition, new data from an exploratory study will be presented which demonstrate the impact of Lemtrada on retinal nerve fibers.

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Lemtrada Investigational Brain Volume Data: Relapsing-remitting multiple sclerosis (RRMS) patients treated with interferon beta-1a in CARE-MS I and II for two years who switched to Lemtrada in the extension study experienced a reduced rate of brain volume loss over the next three years.

Median yearly brain volume loss in interferon beta-1a treated patients in year two in CARE-MS I (-0.50%) and CARE-MS II (-0.33%) was reduced in years one, two and three after switching to Lemtrada (CARE-MS I: -0.07%, -0.13%, -0.09%; CARE-MS II: 0.02%, -0.05%, -0.14%).

Lemtrada Investigational Retinal Data: A measurable improvement in retinal nerve fiber layer (RNFL) thickness was seen in 26 Lemtrada-treated RRMS patients. Over two years, the change in average RNFL thickness for all eyes was +1.5 micrometers (95% CI 0.2, 2.9; p=0.032). The observed thickening of retinal fibers may reflect protection of retinal axons in these patients.

"The Lemtrada data being presented at AAN from the ongoing extension study demonstrating slowed brain volume loss over three years are consistent with sustained effects seen in prior clinical, imaging and atrophy analyses," said Dr. Anthony Traboulsee, Associate Professor of Neurology and Medical Director of the UBC Hospital MS Clinic of Vancouver Coastal Health. "In addition, given the critical importance of neuroprotection in the treatment of MS, the retinal nerve fiber data are also exciting and support further investigation."

In clinical trials, serious side effects associated with Lemtrada included infusion-associated reactions, autoimmune disorders (such as thyroid disease, autoimmune cytopenias, and nephropathies), infections and pneumonitis. Risk management programs incorporating education and monitoring help support early detection and management of key identified and potential risks. The most common side effects of Lemtrada are rash, headache, pyrexia, nasopharyngitis, nausea, urinary tract infection, fatigue, insomnia, upper respiratory tract infection, herpes viral infection, urticaria, pruritus, thyroid gland disorders, fungal infection, arthralgia, pain in extremity, back pain, diarrhea, sinusitis, oropharyngeal pain, paresthesia, dizziness, abdominal pain, flushing, and vomiting. (See Important Safety Information below.)

About Lemtrada (alemtuzumab)
Lemtrada is approved in more than 50 countries, with additional marketing applications under review by regulatory authorities globally. Lemtrada is supported by a comprehensive and extensive clinical development program that involved nearly 1,500 patients worldwide and 5,400 patient-years of follow-up.

In CARE-MS I, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates; the difference observed in slowing disability progression did not reach statistical significance. In CARE-MS II, Lemtrada was significantly more effective than interferon beta-1a at reducing annualized relapse rates, and accumulation of disability was significantly slowed in patients given Lemtrada vs. interferon beta-1a.

The precise mechanism by which alemtuzumab exerts its therapeutic effects in MS is unknown. Alemtuzumab is a monoclonal antibody that targets CD52, a protein abundant on T and B cells. Circulating T and B cells are thought to be responsible for the damaging inflammatory process in MS. Lemtrada depletes circulating T and B lymphocytes after each treatment course. Lymphocyte counts then increase over time with a reconstitution of the lymphocyte population that varies for the different lymphocyte subtypes.

Genzyme holds the worldwide rights to alemtuzumab and has responsibility for its development and commercialization in multiple sclerosis. Bayer Healthcare receives contingent payments based on global sales revenue.

Lemtrada (alemtuzumab) U.S. Indication
LEMTRADA is a prescription medicine used to treat adults with relapsing forms of multiple sclerosis (MS). Because of its risks, LEMTRADA is generally used in people who have tried 2 or more MS medicines that have not worked well enough. It is not known if LEMTRADA is safe and effective for use in children under 17 years of age.

Do not receive LEMTRADA if you are infected with human immunodeficiency virus (HIV).

IMPORTANT SAFETY INFORMATION

LEMTRADA can cause serious side effects including:

Serious autoimmune problems: Some people receiving LEMTRADA develop a condition where the immune cells in your body attack other cells or organs in the body (autoimmunity), which can be serious and may cause death. Serious autoimmune problems may include:

• Immune thrombocytopenia, which is when reduced platelet counts in your blood cause severe bleeding that, if not treated, may cause life-threatening problems. Call your healthcare provider right away if you have any of the following symptoms: easy bruising; bleeding from a cut that is hard to stop; heavier menstrual periods than normal; bleeding from your gums or nose that is new or takes longer than usual to stop; small, scattered spots on your skin that are red, pink, or purple

• Kidney problems called anti-glomerular basement membrane disease, which can, if untreated, lead to severe kidney damage, kidney failure that needs dialysis, a kidney transplant, or death. Call your healthcare provider right away if you have any of the following symptoms: blood in the urine (red or tea-colored urine); swelling of legs or feet; coughing up blood

It is important for you to have blood and urine tests before you receive, while you are receiving and every month, for 4 years or longer, after you receive your last LEMTRADA infusion.

Serious infusion reactions: LEMTRADA can cause serious infusion reactions that may cause death. Serious infusion reactions may happen while you receive, or up to 24 hours or longer after you receive LEMTRADA.

• You will receive your infusion at a healthcare facility with equipment and staff trained to manage infusion reactions, including serious allergic reactions, and urgent heart or breathing problems. You will be watched while you receive, and for 2 hours or longer after you receive, LEMTRADA. If a serious infusion reaction happens while you are receiving LEMTRADA, your infusion may be stopped.

Tell your healthcare provider right away if you have any of the following symptoms of a serious infusion reaction during the infusion, and after you have left the healthcare facility:

• swelling in your mouth or throat

• trouble breathing

• weakness

• fast, slow, or irregular heartbeat

• chest pain

• rash

To lower your chances of getting a serious infusion reaction, your healthcare provider will give you a medicine called corticosteroids before your first 3 infusions of a treatment course. You may also be given other medicines before or after the infusion to try to reduce your chances of having these reactions or to treat them after they happen.

Certain cancers: Receiving LEMTRADA may increase your chance of getting some kinds of cancers, including thyroid cancer, skin cancer (melanoma), and blood cancers called lymphoproliferative disorders and lymphoma. Call your healthcare provider if you have the following symptoms that may be a sign of thyroid cancer:

• new lump

• swelling in your neck

• pain in front of neck

• hoarseness or other voice changes that do not go away

• trouble swallowing or breathing

• cough that is not caused by a cold

Have your skin checked before you start receiving LEMTRADA and each year while you are receiving treatment to monitor for symptoms of skin cancer.

Because of risks of autoimmunity, infusion reactions, and some kinds of cancers, LEMTRADA is only available through a restricted program called the LEMTRADA Risk Evaluation and Mitigation Strategy (REMS) Program.

Thyroid problems: Some patients taking LEMTRADA may get an overactive thyroid (hyperthyroidism) or an underactive thyroid (hypothyroidism). Call your healthcare provider if you have any of these symptoms:

• excessive sweating

• unexplained weight loss

• eye swelling

• nervousness

• fast heartbeat

• unexplained weight gain

• feeling cold

• worsening tiredness

• constipation

Low blood counts (cytopenias): LEMTRADA may cause a decrease in some types of blood cells. Some people with these low blood counts have increased infections. Call your doctor right away if you have symptoms of cytopenias such as:

• weakness

• chest pain

• yellowing of the skin or whites of the eyes (jaundice)

• dark urine

• fast heartbeat

Serious infections: LEMTRADA may cause you to have a serious infection while you receive and after receiving a course of treatment. Serious infections may include:

• Herpes viral infections. Some people taking LEMTRADA have an increased chance of getting herpes viral infections. Take any medicines as prescribed by your healthcare provider to reduce your chances of getting these infections.

• Tuberculosis. Your healthcare provider should check you for tuberculosis before you receive LEMTRADA.

• Hepatitis. People who are at high risk of, or are carriers of, hepatitis B (HBV) or hepatitis C (HCV) may be at risk of irreversible liver damage.

These are not all the possible infections that could happen while on LEMTRADA. Call your healthcare provider right away if you have symptoms of a serious infection such as fever or swollen glands. Talk to your healthcare provider before you get vaccinations after receiving LEMTRADA. Certain vaccinations may increase your chances of getting infections.

Swelling of lung tissue (pneumonitis): Some people have had swelling of the lung tissue while receiving LEMTRADA. Call your healthcare provider right away if you have the following symptoms:

• shortness of breath

• cough

• wheezing

• chest pain or tightness

• coughing up blood

Before receiving LEMTRADA, tell your healthcare provider if you:

• are taking a medicine called Campath (alemtuzumab)

• have bleeding, thyroid, or kidney problems

• have HIV

• have a recent history of infection

• have received a live vaccine in the past 6 weeks before receiving LEMTRADA or plan to receive any live vaccines. Ask your healthcare provider if you are not sure if your vaccine is a live vaccine

• are pregnant or plan to become pregnant. LEMTRADA may harm your unborn baby. You should use birth control while receiving LEMTRADA and for 4 months after your course of treatment

• are breastfeeding or plan to breastfeed. You and your healthcare provider should decide if you should receive LEMTRADA or breastfeed. You should not do both.

Tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. LEMTRADA and other medicines may affect each other, causing side effects. Especially tell your healthcare provider if you take medicines that increase your chance of getting infections, including medicines used to treat cancer or to control your immune system.

The most common side effects of LEMTRADA include:

• rash

• headache

• thyroid problems

• fever

• swelling of your nose and throat

• nausea

• urinary tract infection

• feeling tired

• trouble sleeping

• upper respiratory infection

• herpes viral infection

• hives

• itching

• fungal infection

• joint pain

• pain in your arms or legs

• back pain

• diarrhea

• sinus infection

• mouth pain or sore throat

• tingling sensation

• dizziness

• stomach pain

• sudden redness in face, neck, or chest

• vomiting

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

You are encouraged to report side effects of prescription drugs to the FDA. Visit View Source or call 1-800-FDA-1088

Please click here for full U.S. Prescribing Information, including boxed WARNING and Medication Guide, for additional Important Safety Information

On April 18, 2016 Onxeo S.A. (Euronext Paris, Nasdaq Copenhagen: ONXEO), an innovative company specializing in the development of orphan oncology therapeutics, reported the final data from a study aiming to confirm the mechanism of action of Livatag, a doxorubicin loaded nanoparticle formulation based on Onxeo’s Transdrug technology in overcoming cellular resistance in hepatocellular carcinoma (HCC) (Press release, Onxeo, APR 18, 2016, View Source [SID:1234511024]). Livatag is currently being evaluated in a Phase III trial (ReLive) in patients with advanced HCC, or primary liver cancer.

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Results, presented today in a poster (Abstract #2143 / Poster #13) by Dr. Graham Dixon, PhD, Onxeo’s Chief Scientific Officer, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, demonstrated that the bio-distribution of doxorubicin Transdrug (Livatag) nanoparticles showed a preferential affinity for the liver and an increased exposure in plasma compared to free doxorubicin, together supporting the use of Livatag in the treatment of patients suffering from advanced HCC.

While evaluating the mechanism of action the study showed that the nanoparticle formulation of doxorubicin Transdrug (Livatag) entered into HCC cell lines via passive diffusion and avoided recognition by certain multi-drug resistance (MDR) proteins, (P glycoprotein 1, or Pgp) leading to major accumulation of the drug in the cells and a dramatic increase in cytotoxicity in HCC cell lines compared to free doxorubicin.

Further investigations will be performed to test if doxorubicin Transdrug (Livatag) also overcomes resistance induced by other MDR-related proteins expressed by HCC cells as well as the involvement of the Livatag nanoparticle "ion pair" in overcoming the efflux-mediated resistance.

Graham Dixon, PhD, Chief Scientific Officer of Onxeo, commented, "These are important findings as they confirm that the underlying mechanism of action of Livatag’s nanoformulation effectively accumulates doxorubicin specifically in the liver and evades tumor cell resistance mediated by multiple drug resistance MDR efflux pumps, enabling an efficacious and safe approach to cancer treatment. These results further support our ongoing Phase 3 ReLive study of Livatag for the treatment of patients with advanced HCC, for which we anticipate preliminary data readout mid-2017."