On April 18, 2016 Five Prime Therapeutics, Inc. (Nasdaq:FPRX), a clinical-stage biotechnology company focused on discovering and developing innovative immuno-oncology protein therapeutics, reported that new preclinical data on FPA144 were featured today in a poster presentation from 8 AM to 12 PM (CDT) during the 2016 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, being held April 16-20, in New Orleans (Press release, Five Prime Therapeutics, APR 18, 2016, View Source [SID:1234510972]).

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The poster titled "FPA144, a Therapeutic Monoclonal Antibody Targeting the FGFR2b Receptor, Promotes Antibody Dependent Cell-Mediated Cytotoxicity and Stimulates Sensitivity to PD-1 in the 4T1 Breast Tumor Model in Mice" will be made available on the publications page of the Five Prime website.

"The ability of FPA144 to both recruit and drive an innate response with NK cells followed by an adaptive response with T cells is new and striking biology," said Drew Pardoll, M.D., Ph.D., Seraph Professor of Oncology, Medicine, Pathology and Molecular Biology and Genetics at the Johns Hopkins University of Medicine. "Driving this immune cascade in a patient’s tumor could provide a new therapeutic mechanism for treating solid tumors."

FPA144 is an FGFR2b-specific humanized monoclonal antibody designed to treat patients with cancers that overexpress FGFR2b. FPA144 is a targeted immunotherapy that Five Prime engineered to recruit NK cells into the tumor microenvironment and kill cancer cells by antibody-dependent cell-mediated cytotoxicity (ADCC).

"We are excited by the results we’ve seen in this model. Surprisingly, they suggest that FPA144 can drive an anti-tumor response that involves multiple immune cell types. The upregulation of PD-L1 suggests that combination with an anti-PD-1 agent could yield even more activity," said Robert Sikorski, M.D., Ph.D., Senior Vice President of Global Clinical Development at Five Prime. "Based on these results and the preliminary clinical data we reported in January, we are considering opportunities to evaluate FPA144 in immuno-oncology combination therapies and in tumors types beyond gastric cancer, including those with moderate levels of FGFR2b expression."

Five Prime evaluated the immune cell recruitment and anti-tumor effects of FPA144 in the orthotopic 4T1 model of breast cancer. In this model, the FGFR2 gene is not amplified and tumor cells express only moderate levels of FGFR2b. Doses of FPA144 or FPA144 N297Q (a modified antibody lacking Fc effector function) were administered at Day 0 and Day 3 and tumor histology and FACS were conducted at Day 1 and Day 4. The following was observed with FPA144 treatment:

24 Hours Post 1st Dose 24 Hours Post 2nd Dose
NK cell infiltration within the tumor Persistence of NK cells
Increase in PD-L1-positive cells within the tumor Persistence of PD-L1-positive cells
No change in T cells Increase in T cells within the tumor

Furthermore, therapeutic treatment with FPA144 in this model resulted in a reduction in tumor burden (33%, P < 0.001), while FPA144 N297Q neither inhibited tumor growth nor led to the recruitment of NK cells. These data provide further evidence of the ability of FPA144 to increase NK and T cell numbers within a tumor and suggest that its enhanced ADCC activity may play an important mechanistic role in anti-tumor efficacy in cancers with modest FGFR2b expression.

Additionally, the 4T1 model was used to evaluate the anti-tumor effect of FPA144 alone and in combination with an anti-PD-1 antibody (RMP1-14). Following biweekly dosing, tumor volume was assessed at day 19. Although anti-PD-1 treatment alone did not inhibit tumor growth, treatment with anti-PD-1 in combination with FPA144 inhibited tumor growth by 49% (P < 0.001). Collectively, these results suggest that FPA144 alters the immune cell composition of the tumor microenvironment in a way that primes the tumor to respond to anti-PD-1 therapy, and an additive anti-tumor effect is observed when FPA144 is combined with PD-1 blockade.

Dose expansion is ongoing in the Phase 1 monotherapy trial of FPA144 in patients with gastric cancer, a disease in which FGFR2b protein overexpression and FGFR2 gene amplification have been associated with poor prognosis. Preliminary data showing anti-cancer activity during the dose escalation portion of the trial were presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Gastrointestinal Cancers Symposium in January 2016. Updated data from the trial have been accepted for oral presentation during the ASCO (Free ASCO Whitepaper) Annual Meeting in June 2016.

About FPA144

FPA144 is an anti-FGF receptor 2b (FGFR2b) humanized monoclonal antibody in clinical development as a targeted immune therapy for tumors that over-express FGFR2b, as determined by a proprietary immunohistochemistry (IHC) diagnostic assay. FPA144 is designed to block tumor growth through two distinct mechanisms. First, it binds specifically to FGFR2b and prevents the binding of certain fibroblast growth factors that promote tumor growth. Second, it has been engineered to drive immune-based killing of tumor cells by antibody-dependent cell-mediated cytotoxicity (ADCC) and the recruitment of natural killer (NK) cells. FGFR2 gene amplification (as identified by FISH) is found in a number of tumors, including in approximately 5% of gastric cancer patients, and is associated with poor prognosis.

On April 18, 2016 Mustang Bio, Inc. ("Mustang"), a Fortress Biotech (NASDAQ: FBIO) Company, reported that two abstracts pertaining to its MB-101 (IL13Rα2-specific CAR-T cells) product candidate in development were selected for presentation at the upcoming American Society of Gene and Cell Therapy 19th Annual Meeting (ASGCT) (Free ASGCT Whitepaper), to be held May 4-7, 2016, at the Marriott Wardman Park Hotel in Washington, DC (Filing, 8-K, Fortress Biotech, APR 18, 2016, View Source [SID:1234510996]).

Pre-clinical Oral Presentation:
· Title: Optimization of IL13Rα2-specific CAR T cells for Clinical Development Using Orthotopic Human Glioblastoma Models in NSG Mice
o Abstract Number: 275
o Session: Oral Abstract Session 243 – Cancer-Immunotherapy, Cancer Vaccines I
o Date and Time: Thursday, May 5, 2016; 4:00 – 5:45 PM ET
o Location: Marriott Wardman Park Hotel, Washington 4
o Presenter: Dr. Christine Brown, Associate Director, T cell Therapeutics Research Laboratory at the City of Hope Medical Center ("COH")

Clinical Oral Presentation:
· Title: Phase I Study of Second Generation Chimeric Antigen Receptor–Engineered T cells Targeting IL13Rα2 for the Treatment of Glioblastoma
o Abstract Number: 247
o Session: Scientific Symposium 201 – Clinical Trials Spotlight
o Date and Time: Thursday, May 5, 2016; 8:00 AM – 10:00 AM ET
o Location: Marriott Wardman Park Hotel, Thurgood Marshall NE
o Presenter: Dr. Benham Badie, Vice Chair and Professor, Department of Surgery, Chief, Division of Neurosurgery, Director, Brain Tumor Program and Neurosurgeon at the City of Hope Medical Center ("COH")

Copies of the above referenced abstracts can be viewed online through the ASGCT (Free ASGCT Whitepaper) meeting website at View Source

About Glioblastoma multiforme (GBM)
Glioblastomas (GBM) are tumors that arise from astrocytes—the star-shaped cells that make up the supportive tissue of the brain. These tumors are usually highly malignant (cancerous) because the cells reproduce quickly and they are supported by a large network of blood vessels. GBM is the most common brain and central nervous system (CNS) malignancy, 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. (Brain Tumor Statistics. American Brain Tumor Association. December 2015). While GBM is a rare disease (2-3 cases per 100,000 person life years in the 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 survival from ~12 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. Treatment is further complicated by the susceptibility of the brain to damage, difficulty of the brain to repair itself and limitation to drugs crossing the blood brain barrier. Immunotherapy approaches targeting brain tumors offer promise over conventional treatments.

About MB-101 (IL13Rα2-specific CAR-T cells)
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 the majority of GBM. CAR-T cells designed to express a membrane-tethered IL-13 receptor ligand (IL-13) incorporating a single point mutation display 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, and extracellular domain of CD19 as a selection/safety marker. In order to further improve persistence, memory T-cells are enriched and genetically engineered using a manufacturing process that limits ex vivo expansion in order to reduce T-cell exhaustion and maintain a memory T-cell phenotype.

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On April 18, 2016 Agendia, Inc., together with the European Organisation for Research and Treatment of Cancer (EORTC) and Breast International Group (BIG), reported results from the initial analysis of the primary objective of the Microarray In Node-negative (and 1 to 3 positive lymph node) Disease may Avoid ChemoTherapy (MINDACT) study at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2016 in, New Orleans, LA (Press release, Agendia, APR 18, 2016, View Source [SID:1234511023]).

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Using the company’s MammaPrint assay, patients with early-stage breast cancer who were considered at high risk for disease recurrence based on clinical and biological criteria had a distant metastasis-free survival at five years in excess of 94 percent. The MammaPrint test—the first and only genomic assay with FDA 510(k) clearance for use in risk assessment for women of all ages with early stage breast cancer—identified a large group of patients for whom five-year distant metastasis–free survival was equally good whether or not they received adjuvant chemotherapy (chemotherapy given post-surgery).

"The MINDACT trial design is the optimal way to prove clinical utility of a genomic assay," said Prof. Laura van ’t Veer, CRO at Agendia, Leader, Breast Oncology Program, and Director, Applied Genomics at UCSF Helen Diller Family Comprehensive Cancer Center. "It gives the level 1A clinical evidence (prospective, randomized and controlled) that empowers physicians to clearly and confidently know when chemotherapy is part of optimal early-stage breast cancer therapy. In this trial, MammaPrint (70-gene assay) was compared to the standard of care physicians use today, to decide what is the best treatment option for an early-stage breast cancer patient."

The MINDACT trial is the first prospective randomized controlled clinical trial of a breast cancer recurrence genomic assay with level 1A clinical evidence and the first prospective translational research study of this magnitude in breast cancer to report the results of its primary objective.

Among the 3,356 patients enrolled in the MINDACT trial, who were categorized as having a high risk of breast cancer recurrence based on common clinical and pathological criteria (C-high), the MammaPrint assay reduced the chemotherapy treatment prescription by 46 percent.Using the 70-gene assay, MammaPrint, 48 percent of lymph-node positive breast cancer patients considered clinically high-risk (Clinical-high) and genomic low-risk (MammaPrint-low) had an excellent distant metastasis-free survival at five years in excess of 94 percent.

"Traditionally, physicians have relied on clinical-pathological factors such as age, tumor size, tumor grade, lymph node involvement, and hormone receptor status to make breast cancer treatment decisions," said Massimo Cristofanilli, MD, Associate Director of Translational Research and Precision Medicine at the Robert H. Lurie Comprehensive Cancer Center, Northwestern University in Chicago. "These findings provide level 1A clinical utility evidence by demonstrating that the detection of low-risk of distant recurrence reported by the MammaPrint test can be safely used in the management of thousands of women by identifying those who can be spared from a toxic and unnecessary treatment."

MINDACT is a randomized phase III trial that investigates the clinical utility of MammaPrint, when compared (or – "used in conjunction with") to the standard clinical pathological criteria, for the selection of patients unlikely to benefit from adjuvant chemotherapy. From 2007 to 2011, 6,693 women who had undergone surgery for early-stage breast cancer enrolled in the trial (111 centers in nine countries). Participants were categorized as low or high risk for tumor recurrence in two ways: first, through analysis of tumor tissue using MammaPrint at a central location in Amsterdam; and second, using Adjuvant! Online, a tool that calculates risk of breast cancer recurrence based on common clinical and biological criteria.

Patients characterized in both clinical and genomic assessments as "low- risk" are spared chemotherapy, while patients characterized as "high- risk" are advised chemotherapy. Those with conflicting results are randomized to use either clinical or genomic risk (MammaPrint) evaluation to decide on chemotherapy treatment.

The MINDACT trial is managed and sponsored by the EORTC as part of an extensive and complex partnership in collaboration with Agendia and BIG, and many other academic and commercial partners, as well as patient advocates.

"These MINDACT trial results are a testament that the science of the MammaPrint test is the most robust in the genomic breast recurrence assay market. Agendia will continue to collaborate with pharmaceutical companies, leading cancer centers and academic groups on additional clinical research and in the pursuit of bringing more effective, individualized treatments within reach of cancer patients," said Mark Straley, Chief Executive Officer at Agendia. "We value the partnership with the EORTC and BIG and it’s a great honor to share this critical milestone."

Breast cancer is the most frequently diagnosed cancer in women worldwide.[i] In 2012, there were nearly 1.7 million new breast cancer cases among women worldwide, accounting for 25 percent of all new cancer cases in women.[ii]

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 Infinity Pharmaceuticals, Inc. (NASDAQ: INFI) reported new preclinical data for IPI-549, an orally administered immuno-oncology development candidate that selectively inhibits phosphoinositide-3-kinase gamma (PI3K-gamma) (Press release, Infinity Pharmaceuticals, APR 18, 2016, View Source;p=RssLanding&cat=news&id=2157820 [SID:1234510975]). Preclinical data in multiple solid tumor models demonstrate that IPI-549 targets immune cells and alters the immune-suppressive microenvironment, promoting an anti-tumor immune response that leads to tumor growth inhibition. Data also demonstrate that IPI-549 enhances the effects of checkpoint inhibitors, resulting in improved survival in murine models. These data were presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2016 in New Orleans, Louisiana. A Phase 1 clinical study is under way to explore the safety and activity of IPI-549 both as a monotherapy and in combination with anti-PD-1 antibody therapy, a type of checkpoint inhibitor.

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"While advances in our understanding of the immune response to cancer have resulted in new therapies for patients, additional treatments are needed that can offer even more patients the chance for prolonged survival," stated Jedd Wolchok, M.D., Ph.D., chief of Melanoma and Immunotherapeutics Service, Lloyd J. Old/Ludwig Chair in Clinical Investigation Department of Medicine and Ludwig Center, at Memorial Sloan Kettering Cancer Center and lead investigator for the Phase 1 clinical study of IPI-549. "Emerging data from our collaboration with Infinity’s discovery team provide additional rationale for combining IPI-549 with checkpoint inhibitors, and I am pleased to be leading the Phase 1 study for this program."

Preclinical Data for IPI-549 Presented at the AACR (Free AACR Whitepaper) Annual Meeting 2016 (Abstract #554)
Infinity researchers, in collaboration with researchers at Memorial Sloan Kettering Cancer Center, presented preclinical data for IPI-549 in a poster entitled, "Checkpoint blockade therapy is improved by altering the immune suppressive microenvironment with IPI-549, a potent and selective inhibitor of PI3K-gamma, in preclinical models."

In preclinical models, treatment with IPI-549 leads to a decrease in tumor-associated immune suppressive myeloid cells. IPI-549 treatment also leads to a decrease in FOXP3 T-regulatory cells, which have immune-suppressive effects, and an increase in intratumoral CD8+ T-cells, which are known to play a role in inhibiting tumor growth. Taken together, these data suggest that through its effect on myeloid cells and T-cells, IPI-549 has the potential to disrupt the immune-suppressive microenvironment and enable a heightened anti-tumor immune response.

Preclinical data in murine models show that treatment with IPI-549 in combination with anti-CTLA4 or anti-PD-L1, two types of checkpoint inhibitors, results in greater tumor growth inhibition compared to monotherapy treatment. Additionally, IPI-549 in combination with anti-PD-1 increased the number of complete responses and improves survival. Re-implantation of tumor cell lines into mice that had achieved complete responses revealed low or no tumor engraftment, suggesting sustained tumor-specific immune protection.

These data provide additional preclinical rationale for the ongoing Phase 1 clinical study designed to explore the safety and activity of IPI-549 as a monotherapy and in combination with anti–PD-1 antibody therapy in patients with selected solid tumors, including non-small cell lung cancer and melanoma (ClinicalTrials.gov identifier NCT02637531).

Infinity is also developing duvelisib, an investigational, oral, dual inhibitor of PI3K-delta and PI3K-gamma. The PI3K pathway is also known to play a critical role in regulating the growth and survival of certain types of blood cancers. Duvelisib is being evaluated in registration-focused studies, including DYNAMOTM, a Phase 2 study in patients with refractory indolent non-Hodgkin lymphoma (iNHL), BRAVURA, a Phase 3 study in patients with relapsed iNHL, and DUOTM, a Phase 3 study in patients with relapsed/refractory chronic lymphocytic leukemia. For additional information about clinical studies of duvelisib, please visit www.infi.com or www.clinicaltrials.gov.

About IPI-549
IPI-549 is an orally administered immuno-oncology development candidate that selectively inhibits PI3K-gamma. In preclinical studies, IPI-549 inhibits immune-suppressive macrophages within the tumor microenvironment, whereas other immunotherapies such as checkpoint modulators more directly target immune effector cell function. As such, IPI-549 may have the potential to treat a broad range of solid tumors and represents a potentially complementary approach to restoring anti-tumor immunity in combination with other immunotherapies such as checkpoint inhibitors.

Duvelisib and IPI-549 are investigational compounds and their safety and efficacy have not been evaluated by the U.S. Food and Drug Administration or any other health authority.