On June 22, 2020 CytomX Therapeutics, Inc. (Nasdaq: CTMX) reported that its partner Bristol Myers Squibb presented preclinical data from BMS-986249 and BMS-986288, anti-CTLA-4 Probody therapeutics generated with CytomX’s novel Probody technology platform (Press release, CytomX Therapeutics, JUN 22, 2020, View Source [SID1234561285]). The electronic poster #4551 titled "Preclinical characterization of novel anti-CTLA-4 prodrug antibodies with an enhanced therapeutic index" was presented as part of the Therapeutic Antibodies 3 Session at the American Association of Cancer Research’s (AACR) (Free AACR Whitepaper) 2020 Virtual Annual Meeting II.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

BMS-986249 is a Probody version of the anti-CTLA-4 antibody ipilimumab (Yervoy). In February 2020, Bristol Myers Squibb treated the first patient in a Part 2a randomized cohort expansion in an ongoing Phase 1/2a trial of BMS-986249 in combination with Opdivo (nivolumab) in patients with metastatic melanoma. Additional information is available at ClinicalTrials.gov using the Identifier NCT03369223.

BMS-986288 is a Probody of a nonfucosylated version of ipilimumab (anti-CTLA-4 NF). In September 2019, Bristol Myers Squibb initiated the dose escalation phase of a Phase 1/2a clinical trial of BMS-986288 administered as monotherapy and in combination with nivolumab in patients with selected advanced solid tumors. Additional information is available at ClinicalTrials.gov using the Identifier NCT03994601.

These Probody programs, designed to optimize the therapeutic index of CTLA-4-directed therapy, arose from the companies’ 2014 worldwide oncology license and collaboration agreement.

"This important work within our Bristol Myers Squibb alliance is aimed at broadening the utility of this foundational immunotherapeutic approach to the treatment of cancer," said Sean McCarthy D.Phil., president, chief executive officer and chairman of CytomX Therapeutics. "We look forward to seeing the full potential of these programs as they continue to advance in the clinic."

On June 22, 2020 The American Association for Cancer Research (AACR) (Free AACR Whitepaper) reported that it has awarded Van Andel Institute Professor Peter W. Laird, Ph.D., Director’s Scholar Stephen B. Baylin, M.D., FAACR, and Associate Professor Hui Shen, Ph.D., 2020 AACR (Free AACR Whitepaper) Team Science Awards for their pivotal roles in the establishment and success of The Cancer Genome Atlas (TCGA), a landmark project that revolutionized our understanding of cancer and that is hailed as an exemplar of scientific collaboration (Press release, Van Andel Institute, JUN 22, 2020, View Source;utm_medium=rss&utm_campaign=2020-aacr-team-science-award [SID1234561308]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The first Team Science Award includes Laird and Baylin as well as other project leaders and individuals who were central to TCGA. The second Team Science Award includes Laird, Baylin and Shen, along with 127 additional members of the current TCGA project team. Awardees will be honored during a special session of the AACR (Free AACR Whitepaper) Virtual Annual Meeting II on Wednesday, June 24.

Stephen Baylin, M.D.

"The insights revealed by TCGA will continue to transform cancer research and treatment for years to come. We are thrilled to join AACR (Free AACR Whitepaper) and the scientific community in celebrating the contributions of Dr. Laird, Dr. Baylin, Dr. Shen and all those who took part in the project," said Peter A. Jones, Ph.D., D.Sc. (hon), VAI Chief Scientific Officer. "TCGA truly is a testament to the power of team science."

Announced in 2005 and completed in 2018, TCGA was a National Cancer Institute and National Human Genome Research Institute-led effort to molecularly map 33 cancer types, including 10 rare cancers.

In all, hundreds of scientists in the U.S. and Canada participated, resulting in detailed analyses of more than 20,000 biospecimens and numerous scientific publications that continue to fuel new breakthroughs and innovations. It has become an invaluable asset for the development of precision therapies and the identification of new drug targets.

Hui Shen, Ph.D.

Following TCGA’s inception, Laird and Baylin established and co-led the epigenetics analyses arm of the project, which cataloged molecular changes that influence cancer risk by altering how genes are expressed rather than the genes themselves. Laird went on to lead epigenetic analyses for TCGA through its completion, as well as the project’s effort to characterize cancers by their molecular subtype.

Laird began working on TCGA while serving as a professor at University of Southern California, and continued when he joined VAI in 2014.

Shen, who also joined VAI from USC in 2014, played a major role in epigenetic data analyses for the project.

Baylin, who co-leads the Van Andel Institute–Stand Up To Cancer Epigenetics Dream Team, holds a primary appointment at Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University. His insight and guidance were central to the genesis and growth of the epigenetics component of TCGA.

"TCGA was a vastly complex undertaking that demonstrated the power of team science initiatives," Laird said. "Each person who worked on the project played a part in its success and in charting future cancer research and therapies built on its findings."

On June 22, 2020 Autolus Therapeutics plc (Nasdaq: AUTL), a clinical-stage biopharmaceutical company developing next-generation programmed T cell therapies, reported preclinical data related to AUTO5 in T cell lymphoma and AUTO6NG in small cell lung cancer, as well as an oral presentation related to AUTO7 in prostate cancer at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Virtual Annual Meeting II on June 22 – 24, 2020 (Press release, Autolus, JUN 22, 2020, View Source [SID1234561325]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"Behind our lead programs AUTO1 in ALL and AUTO3 in DLBCL, we have a number of exciting preclinical product candidates progressing towards the clinic," said Dr Christian Itin, chairman and chief executive officer of Autolus. "These data updates for AUTO5, AUTO6NG and AUTO7 illustrate the strength of our broad and modular cell programming technology to adapt the product properties to the specific tumor type."

"The Autolus R&D team is pleased to be presenting data updates across our preclinical pipeline, highlighting the strength of our in-house cell programming technology. The programs illustrate the utility of the technology for highly selective targeting with AUTO5 in T cell lymphoma as well as addressing the hostile solid tumor microenvironment with AUTO6NG and AUTO7 for the treatment of small cell lung cancer and prostate cancer, respectively," said Dr Martin Pulé, chief scientific officer and founder of Autolus. "We look forward to progressing these next generation preclinical programs into the clinic in 2021."

AUTO7: Anti-PSMA humanized CAR T cell with improved persistence and resistance to tumor microenvironment for metastatic castration resistant prostate cancer (mCRPC)
AUTO7 is a multi-modular CAR T cell program aimed at generating resilient CAR T cells that can withstand the hostile solid tumor microenvironment (TME). By introducing Autolus’ proprietary programming modules, the new data demonstrate a positive effect on tackling the complex tumor biology in a metastatic, castration-resistant prostate cancer setting. AUTO7 uses an optimized CAR to target cancer cells expressing PSMA, even at low levels, and includes four of Autolus’ suite of cell programming modules to overcome tumor defenses and enhance efficacy: the dSHP2 programming module shielding AUTO7 from checkpoint inhibition, the dominant negative TGFβRII module acting as a decoy for inhibitory TGFβ signaling, the IL7 chimeric cytokine receptor (CCR) module enhancing CAR T cell survival, and finally, a module that activates immune responses at the tumor site through limited secretion of IL-12. All programming modules provide their effect within the CAR T cell and the immediate surrounding environment, rather than having a systemic effect with its potential associated systemic toxicities.

The preclinical data presented by Autolus demonstrate that AUTO7 is highly potent in cytotoxicity assays against cells expressing PSMA, even at low levels, and demonstrate the feasibility of this multi-modular cell programming approach in overcoming the immunotherapeutic challenges presented by advanced prostate cancer, which is typically otherwise an immunologically cold tumor.

Oral Presentation Title: AUTO7: Anti-PSMA humanized CAR T cell with improved persistence and resistance to tumor microenvironment for metastatic castration resistant prostate cancer (mCRPC)
Session Title: Mini-symposium; MS.IM02.01 – Adoptive Cell Therapy
Abstract: 1070
Date & Time: June 23, 2020, 9:00 AM – 10:30 AM
Presenter: Dr Marco Della Peruta, Senior Scientist II, Immunobiology, Autolus Therapeutics

AUTO6NG overcomes immune suppressive mechanisms in the TME and demonstrate preclinical anti-tumor activity in GD2-expressing solid tumors
AUTO6 is a GD2-targeting CAR T candidate, developed in collaboration with UCL, that has been shown to be clinically active in neuroblastoma.* GD2 has been evaluated and validated as an attractive CAR T target antigen in small cell lung cancer (SCLC). AUTO6 alone has demonstrated efficacy in an in vitro SCLC model, but successful tumor targeting alone was not sufficient to drive in vivo efficacy in the same SCLC model. Autolus has designed enhancing modules to specifically overcome TME defenses in solid tumor settings. In addition to the original AUTO6 GD2 CAR and safety switch, the company has tested the impact of adding its dSHP2 module, its dominant negative TGFβRII module and its IL7 CCR module, as described above. Autolus has presented new preclinical data demonstrating the validity of GD2 as a CAR T target in SCLC and the ability of these efficacy-enhancing modules to drive in vivo efficacy in an SCLC mouse model. The new data presented by Autolus suggest that AUTO6NG can overcome the immune suppressive mechanisms in the TME.

*AACR 2018 presentation of AUTO6 clinical data, Dr Karin Straathof, UCL

Poster Presentation Title: AUTO6NG overcomes immune suppressive mechanisms in the TME and demonstrate preclinical anti-tumor activity in GD2-expressing solid tumors
Poster Session Title: Poster Session; PO.TB06.05 – Immune Cells in the Tumor Microenvironment 2
Poster: 2661 / 9
Date & Time: June 22, 2020, 9:00 AM – 6:00 PM
Presenter: Dr Muhammad Al-Hajj, Senior Vice President, Head of Translational Medicine, Autolus Therapeutics

AUTO5: Targeting TRBC2 for the treatment of T cell lymphomas
There is currently no approved programmed T cell therapy available as a stand-alone treatment for T cell lymphomas. AUTO4 is the company’s TRBC1 CAR T cell candidate aimed at targeting TRBC1+ patients (approximately 40% of the T cell lymphoma population). AUTO5, a novel CAR T candidate targeting the TRBC2+ population, is designed to capture the remaining 60% of the T cell lymphoma population. Autolus has presented data showing that AUTO5 is able to selectively target TRBC2+ and spare TRBC1+ cells in a mixed healthy peripheral blood mononuclear cells (PBMC) population. The company demonstrates that its novel anti-TRBC2 binder incorporated in a second-generation CAR with optimized architecture can selectively kill TRBC2+ T cells of healthy PBMC donors. Alongside the killing efficiency, AUTO5 is also capable of specific cytokine release and proliferation in response to interaction with TRBC2 target cells. The same specific killing effect was observed in vivo when mice were challenged in a co-infused mixed TRBC1/TRBC2 tumor model. The anti-TRBC2 CAR was able to clear the TRBC2+ T cells, while sparing the TRBC1+ T cell population. These data highlight the specificity and selectivity of the company’s T-cell lymphoma product candidate, AUTO5.

Poster Presentation Title: Targeting TRBC1 and 2 for the treatment of T cell lymphomas
Poster Session Title: Poster Session; PO.IM02.02 – Adoptive Cell Therapy 2
Poster: 2183 / 15
Date & Time: June 22, 2020, 9:00 AM – 6:00 PM
Presenter: Dr Mathieu Ferrari, Associate Director of Binder Discovery, Autolus Therapeutics

Investor call on Thursday, June 25, 2020
Management will host a conference call and webcast at 8:30 AM EDT/1:30 PM BST to discuss the AACR (Free AACR Whitepaper) data. To listen to the webcast and view the accompanying slide presentation, please go to: View Source

The call may also be accessed by dialing (866) 679-5407 for U.S. and Canada callers or (409) 217-8320 for international callers. Please reference conference ID 1866794. After the conference call, a replay will be available for one week. To access the replay, please dial (855) 859-2056 for U.S. and Canada callers or (404) 537-3406 for international callers. Please reference conference ID 1866794.

On June 22, 2020 ImmunSYS, Inc., a clinical-stage biopharmaceutical company focused on the development of innovative cancer immunotherapy products, reported results from a proof of concept (PoC) study evaluating its proprietary technology platform, YourVaccx for the treatment of patients with metastatic cancers (Press release, ImmunSYS, JUN 22, 2020, View Source [SID1234561341]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The retrospective, IRB approved case series was independently monitored by a contract research organization. A total of 27 patients were enrolled, including 21 with metastatic prostate cancer (mPCa), and 6 with metastatic cancers of varying types: 2 bladder, 1 pancreatic, 1 melanoma, 1 colon cancer and 1 unknown. A single treatment cycle consisted of in situ cryosurgical lysis of tumor tissue followed by a direct injection of a combination of anti CTLA-4 antibody, anti PD-1 antibody and GM-CSF into the target treatment zone, followed by 30 days of daily subcutaneous GM-CSF. The patients were assessed after the completion of therapy, which varied from between 1 and 3 cycles of treatment. All responses to therapy were assessed by RECIST v. 1.1 and metastatic prostate cancer patients were also assessed by serum PSA levels. 3 patients could not be evaluated due to a lack of follow-up imaging. For all evaluable patients, the PoC study data showed a 38% (9/24) complete response rate (CR) and a 4% (1/24) partial response rate (PR), for an objective response rate (ORR) of 42% (10/24). The combination therapy was generally well tolerated.

Key findings in mPCa patients:

Among the 18 evaluable mPCa patients, there was a 50% (9/18) CR
50% (9/18) ORR
62% (13/21) of patients had post-therapy PSA reductions of ≥ 50%
The majority of responses have been durable, with 5 of 9 CRs persisting from 12 months to over 51 months to date
6 Grade 3-4 adverse events occurred in 14.3% (3/21), with no treatment-related deaths
"We are pleased to present these encouraging findings at the AACR (Free AACR Whitepaper) virtual annual meeting II," said Eamonn Hobbs, Chairman and Chief Executive Officer of ImmunSYS. "These results demonstrate long-term, durable responses, ranging from 1 to 4.5 years, and a favorable tolerability profile in tough-to-treat patient populations. There is an unmet need for effective treatment options for patients with metastatic cancers and these data demonstrate the potential that YourVaccx has to significantly improve the lives of patients."

Our poster #6540 entitled, "Regression of metastatic cancer and abscopal effects following in situ vaccination by cryosurgical tumor cell lysis and intratumoral immunotherapy: A case series" and accompanying audio clip narrated by Gary Onik, M.D. is now available at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2020 Virtual Annual Meeting II.

For more information, a copy of the poster may be found on www.immunsys.com

On June 222, 2020 Verastem, Inc. (Nasdaq:VSTM) (also known as Verastem Oncology), a biopharmaceutical company committed to developing and commercializing new medicines for patients battling cancer, reported results from a study that provides preclinical proof-of-concept for combining VS-6766, its RAF/MEK inhibitor, with defactinib, its focal adhesion kinase (FAK) inhibitor, for the treatment of metastatic uveal melanoma (UM), the most prevalent eye cancer among adults (Press release, Verastem, JUN 22, 2020, View Source [SID1234561357]). The data comprise one of four virtual posters with Verastem authors being presented today at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2020 Virtual Annual Meeting II, which is taking place June 22-24, 2020.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Uveal melanoma arises from the melanin-producing cells in the eye, similar to how it arises in cutaneous melanoma. While it’s considered rare, primary UM metastasizes in 50% of patients with only 8% of patients surviving 2 years after development of metastatic disease.1 Previously, MEK inhibitors, including selumetinib and trametinib, have failed to show substantial clinical benefit for patients with metastatic uveal melanoma.2,3 Indeed, no current therapies improve overall survival for metastatic UM and there is a high unmet need for novel therapies.4

In the current preclinical study, FAK inhibition (FAKi; e.g., defactinib) demonstrated synergistic growth-inhibitory effects in UM cells when combined with a MEK inhibitor (MEKi) or the investigational RAF/MEK inhibitor VS-6766. Additionally, MEKi increased phosphorylation of FAK, suggesting the need for FAK blockade in combination with MEKi for more complete antitumor effect. Accordingly, FAKi combination with MEKi induced apoptotic cell death leading to rapid tumor regression in UM xenografts, whereas the MEKi or FAKi as single agents showed tumor growth inhibition but failed to showed tumor shrinkage. Furthermore, the FAKi/MEKi combination was successful at reducing tumor burden in liver metastasis UM models.

"The study identified and reinforced FAK as a viable pathway to inhibit downstream from the GNAQ pathway, which is constitutively active in UM," said J. Silvio Gutkind, PhD, Distinguished Professor of Pharmacology and Associate Director for Basic Science at UC San Diego Moores Cancer Center, and senior investigator of the study. "We observed that co-targeting of FAK and RAF/MEK signaling led to tumor collapse in UM xenograft and liver metastasis models in vivo. Based on the encouraging results of this study, we are excited to work toward clinical testing of defactinib with VS-6766 for patients with metastatic uveal melanoma."

"These data build on a growing body of evidence that underscore the potential of the VS-6766/defactinib combination for treatment of a variety of solid tumors with significant medical need," said Brian Stuglik, Chief Executive Officer of Verastem Oncology. "We will continue to evaluate the combination in metastatic uveal melanoma along with rapidly advancing our broader clinical development program in solid tumors."

The combination of VS-6766 and defactinib is being evaluated in patients with Low Grade Serous Ovarian Cancer (LGSOC), and KRAS mutant non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) in the ongoing investigator-initiated Phase I trial. The company also plans to support a Phase II investigator-initiated study of the combination of VS-6766 and defactinib in uveal melanoma anticipated to begin in late 2020.

Details for all abstracts selected for presentation at the AACR (Free AACR Whitepaper) 2020 Virtual Meeting II are as follows:

Title: FAK and MEK co-targeting: A new multimodal precision therapy for GNAQ-driven uveal melanoma
Lead author: Justine S. Paradis
Poster #: 6406/30
Session: PO.ET06.05
Date and Time: Monday, June 22, 2020; 9:00 a.m. to 6:00 p.m. EDT
URL: View Source!/9045/presentation/5323

Title: The dual PI3K-δ/PI3K-γ inhibitor duvelisib inhibits signaling and proliferation of solid tumor cells expressing PI3K-δ and/or PI3K-γ
Lead author: Silvia Coma
Poster #: 663/10
Session: PO.ET06.06
Date and Time: Monday, June 22, 2020; 9:00 a.m. to 6:00 p.m. EDT
URL: View Source!/9045/presentation/1880

Title: Single cell expression analysis of PIK3 genes to direct solid tumor treatment with the dual PI3K-δ,γ inhibitor duvelisib
Lead author: Samantha Hidy
Poster #: 1552/3
Session: PO.TB06.02
Date and Time: Monday, June 22, 2020; 9:00 a.m. to 6:00 p.m. EDT
URL: View Source!/9045/presentation/7806

Title: PEGylated recombinant human hyaluronidase, PEGPH20, significantly enhances the anti-tumor activity of the combination of focal adhesion kinase Inhibitor and anti-PD-1 antibody by targeting CXCR4-expressing myeloid cells in a murine model of PDAC
Lead author: Arsen Osipov
Poster #: 1588/9
Session: PO.TB06.04
Date and Time: Monday, June 22, 2020; 9:00 a.m. to 6:00 p.m. EDT
URL: View Source!/9045/presentation/7864

About VS-6766

VS-6766 (formerly known as CH5126766, CKI27 and RO5126766) is a unique inhibitor of the RAF/MEK signaling pathway. In contrast to other MEK inhibitors in development, VS-6766 blocks both MEK kinase activity and the ability of RAF to phosphorylate MEK. This unique mechanism allows VS-6766 to block MEK signaling without the compensatory activation of MEK that appears to limit the efficacy of other inhibitors. The combination of VS-6766 and the focal adhesion kinase (FAK) inhibitor defactinib is currently being investigated in an investigator-initiated Phase 1 dose escalation and expansion study. The expansion cohorts are currently ongoing in patients with KRAS mutant advanced solid tumors, including low grade serous ovarian cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal cancer (CRC).6 The ongoing clinical study of the VS-6766/defactinib combination is supported by single-agent Phase 2 studies which investigated defactinib in KRAS mutant NSCLC7 and VS-6766 in KRAS mutant NSCLC and LGSOC.5

About Defactinib

Defactinib (VS-6063) is an oral small molecule inhibitor of FAK and PYK2 that is currently being evaluated as a potential combination therapy for various solid tumors. The Company has received Orphan Drug designation for defactinib in ovarian cancer and mesothelioma in the US, EU and Australia. Preclinical research by Verastem Oncology scientists and collaborators at world-renowned research institutions has described the effect of FAK inhibition to enhance immune response by decreasing immuno-suppressive cells, increasing cytotoxic T cells, and reducing stromal density, which allows tumor-killing immune cells to enter the tumor.8,9 Additionally, in both preclinical and clinical studies, FAK activation has been shown to occur as a potential resistance mechanism in response to MEK inhibitor treatment, and synergy of a FAK inhibitor with a RAF/MEK inhibitor has been shown in several preclinical models. The combination of defactinib and VS-6766 is currently being investigated in an investigator-initiated Phase 1 dose escalation and expansion study. The expansion cohorts are currently ongoing in patients with KRAS mutant advanced solid tumors, including low grade serous ovarian cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal cancer (CRC).6 The ongoing clinical study of the VS-6766/defactinib combination is supported by single-agent Phase 2 studies which investigated defactinib in KRAS mutant NSCLC7 and VS-6766 in KRAS mutant NSCLC and LGSOC.8 Defactinib is also in clinical testing in combination with pembrolizumab for treatment of patients with pancreatic cancer, NSCLC and mesothelioma.10

About COPIKTRA (duvelisib)

COPIKTRA is an oral inhibitor of phosphoinositide 3-kinase (PI3K), and the first approved dual inhibitor of PI3K-delta and PI3K-gamma, two enzymes known to help support the growth and survival of malignant B-cells. PI3K signaling may lead to the proliferation of malignant B-cells and is thought to play a role in the formation and maintenance of the supportive tumor microenvironment.11,12,13 COPIKTRA is indicated for the treatment of adult patients with relapsed or refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) after at least two prior therapies and relapsed or refractory follicular lymphoma (FL) after at least two prior systemic therapies. COPIKTRA is also being developed by Verastem Oncology for the treatment of peripheral T-cell lymphoma (PTCL), for which it has received Fast Track status and Orphan Drug Designation, and is being investigated in combination with other agents through investigator-sponsored studies.14 For more information on COPIKTRA, please visit www.COPIKTRA.com. Information about duvelisib clinical trials can be found on www.clinicaltrials.gov.