TRILLIUM THERAPEUTICS’ TTI-621 PROGRAM FEATURED AT THE EORTC CLTF CUTANEOUS LYMPHOMA CONFERENCE

On October 16, 2017 Trillium Therapeutics Inc. (NASDAQ/TSX: TRIL), a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, reported that new preclinical data and a patient case study for its CD47-blocking agent, TTI-621 (SIRPa-IgG1 Fc), were presented at the EORTC CLTF meeting “Cutaneous Lymphomas – Insights and Therapeutic Progress”, October 13-15, in London, England (Press release, Trillium Therapeutics, OCT 16, 2017, View Source [SID1234520954]).

Oral Presentation O-16: CD47 Blockade with TTI-621 (SIRPαFc) in Sézary Syndrome

Presenter: Dr. Oleg Akilov, University of Pittsburgh

This oral presentation highlighted that leukemic cells from patients with Sézary syndrome, a form of cutaneous T cell lymphoma (CTCL), express the CD47 “do not eat” signal at almost four times the level of normal lymphocytes and that over-expression of CD47 is associated with poor prognosis. In vitro experiments demonstrated that blockade of CD47, employing TTI-621, may constitute a promising therapeutic approach for patients with Sézary syndrome. Two clinical trials of TTI-621 that include patients with relapsed or refractory CTCL are ongoing at multiple North American sites (NCT02663518 and NCT02890368).

Poster Presentation P-10: Synergistic Effect of Successive Administration of TTI-621 (SIRPαFc) and PEGylated Interferon-α2a in a Patient with Sézary Syndrome

Presenter: Dr. Oleg Akilov, University of Pittsburgh

This case study reported local and systemic anti-tumor activity in a Sézary syndrome patient treated with a single intratumoral dose of TTI-621. Administration of PEGylated Interferon-α2a seven days after TTI-621 resulted in decreased leukemic burden and improvements in clinical symptoms. Trillium believes such a reduction is not observed regularly with standard regimens and would not be anticipated following PEGylated Interferon-α2a monotherapy, suggesting a synergistic effect of TTI-621 and PEGylated Interferon-α2a.

“CTCL patients are being treated in both our intratumoral and intravenous trials,” said Dr. Niclas Stiernholm, Trillium’s Chief Executive Officer. “Careful study of the effects of TTI-621 in CTCL patients potentially provides us with a unique opportunity to better understand the mechanism behind TTI-621’s anti-tumor activity and the role of CD47 in the overall immuno-oncology landscape, ultimately leading to targeted indications and combination therapies with sound scientific rationale.”

About Cutaneous T-Cell Lymphoma (CTCL)

CTCL is a rare type of non-Hodgkin’s lymphoma which is characterized by localization of malignant T lymphocytes to the skin. The two most common types of CTCL are mycosis fungoides and Sézary syndrome. The disease most often involves the skin, may progress to involve lymph nodes, blood, viscera and other organs, and in select cases may become leukemic.

Pfizer Presents Full Results from Phase 2 Study of Next-Generation Investigational ALK-Inhibitor Lorlatinib in ALK-Positive and ROS1-Positive Advanced Non-Small Cell Lung Cancer

On October 16, 2017 Pfizer Inc. (NYSE:PFE) reported full results from the Phase 2 clinical trial of the investigational, next-generation tyrosine kinase inhibitor lorlatinib that exhibited clinically meaningful activity against lung tumors and brain metastases in a range of patients with ALK-positive and ROS1-positive advanced non-small cell lung cancer (NSCLC), including those who were heavily pretreated (Press release, Pfizer, OCT 16, 2017, View Source [SID1234520950]). Further, side effects were generally manageable and primarily mild to moderate in severity. The results [Abstract #OA 05.06] were presented by Professor Benjamin Solomon, lead investigator and medical oncologist at Peter MacCallum Cancer Centre, Melbourne, Australia, today during an oral session at the International Association for the Study of Lung Cancer (IASLC) 18th World Conference on Lung Cancer (WCLC) in Yokohama, Japan. Pfizer will also present data from several other lung cancer clinical programs.

“The findings presented today suggest that lorlatinib, if approved, may represent an effective treatment option for patients with ALK-positive advanced non-small cell lung cancer across multiple lines of therapy. These are comprehensive data in non-small cell lung cancer patients previously treated with second-generation ALK inhibitors who currently have few available treatment options,” said Professor Benjamin Solomon, lead investigator and medical oncologist at Peter MacCallum Cancer Centre, Melbourne, Australia. “Controlling brain metastases is very important to these patients and an especially challenging aspect of treating this disease. We saw excellent intracranial responses in all patient groups, including those who were heavily pretreated.”

“Lorlatinib is an extraordinary example of what can be achieved through translational research and precision medicine development. Recall that Xalkori (crizotinib) was the first drug approved for patients with ALK-positive and ROS1-positive NSCLC. By understanding the mutations that occurred in patients that rendered their tumors resistant to Xalkori and other ALK inhibitors, medicinal chemists working at Pfizer were able to design a molecule with the potential to overcome that resistance and inhibit ALK despite these mutations. We are very encouraged by the results of this Phase 2 trial that provide the first clinical evidence of the activity of lorlatinib in this setting,” said Mace Rothenberg, MD, chief development officer, Oncology, Pfizer Global Product Development.

The Phase 2 study examined the antitumor activity and safety of lorlatinib in 275 patients with or without asymptomatic, untreated or treated brain metastases. Patients were enrolled in six cohorts based on biomarker (ALK-positive or ROS1-positive) and prior therapy. The primary endpoints were objective response rate (ORR) and intracranial ORR (IC-ORR) confirmed by independent central review (ICR). Results by clinically relevant groups showed:

ALK-positive treatment-naïve: ORR was 90% (27/30; 95% CI: 74, 98) and IC-ORR was 75% (6/8; 95% CI: 35, 97).
ALK-positive previously treated with crizotinib with or without chemotherapy: ORR was 69% (41/59; 95% CI: 56, 81) and IC-ORR was 68%(25/37; 95% CI: 50, 82).
ALK-positive previously treated with a non-crizotinib ALK inhibitor with or without chemotherapy: ORR was 33% (9/27; 95% CI: 16, 54) and IC-ORR was 42% (5/12; 95% CI: 15, 72).
ALK-positive previously treated with two or three prior ALK inhibitors with or without chemotherapy: ORR was 39% (43/111; 95% CI: 30, 49) and IC-ORR 48% (40/83; 95% CI: 37, 59).
ROS1-positive regardless of prior treatment: ORR was 36% (17/47; 95% CI: 23, 52) and IC-ORR was 56% (14/25; 95% CI: 35, 76).
Lorlatinib was generally tolerable. Most adverse events were mild to moderate and were managed by dose reductions or delay or with standard medical therapy. There were no treatment-related deaths and a low (3%) rate of discontinuation due to drug-related adverse events. The most common adverse events were: hypercholesterolemia (81%), hypertriglyceridemia (60%), edema (43%), peripheral neuropathy (30%), weight increase (18%), cognitive effects (18%), mood effects (15%), fatigue (13%), diarrhea (11%), arthralgia (10%), and increased AST (10%).

The Phase 2 data will form the basis of discussions with global regulatory authorities, including the U.S. Food and Drug Administration. On April 26, 2017, the FDA granted Breakthrough Therapy designation for lorlatinib for the treatment of patients with ALK-positive metastatic NSCLC previously treated with one or more ALK inhibitors.

Pfizer Oncology continues to build on its heritage in biomarker-driven therapies by investigating novel targeted therapies and immunotherapy combination approaches aimed at addressing significant unmet needs for patients. In addition to the lorlatinib results, Pfizer will present data at the conference from studies examining its current and investigational lung cancer medicines:

Plasma genomic profiling and outcomes of patients with MET exon-14 altered NSCLC treated with crizotinib on PROFILE 1001 (Late-breaker oral presentation: Abstract #OA 12.06)
First-line dacomitinib versus gefitinib in advanced non-small cell lung cancer with EGFR mutation subgroups (Oral presentation: Abstract #OA 05.01)
Next-generation sequencing shows mechanisms of intrinsic resistance in ALK-positive NSCLC patients treated with crizotinib (Poster presentation: Abstract #P1.01-016)
Dacomitinib versus gefitinib for first-line treatment of advanced EGFR NSCLC in Japanese patients (ARCHER 1050) (Poster presentation: Abstract #P3.01-072)
Symptom impact of first-line dacomitinib versus gefitinib in EGFR-positive NSCLC: Results from a randomized phase 3 study (Poster presentation: Abstract #P3.01-012)
About Non-Small Cell Lung Cancer

Lung cancer is the leading cause of cancer death worldwide.1 NSCLC accounts for about 85 percent of lung cancer cases and remains difficult to treat, particularly in the metastatic setting.2 Approximately 75 percent of NSCLC patients are diagnosed late with metastatic or advanced disease where the five-year survival rate is only five percent.2,3,4

About Lorlatinib

Lorlatinib is an investigational next-generation ALK/ROS1 tyrosine kinase inhibitor that has been shown to be highly active in preclinical lung cancer models harboring chromosomal rearrangements of both ALK and ROS1. Lorlatinib was specifically designed to inhibit tumor mutations that drive resistance to other ALK inhibitors and to penetrate the blood brain barrier.

The Phase 3 CROWN study (NCT03052608) of lorlatinib began enrolling patients earlier this year. CROWN is an ongoing, open label, randomized, two-arm study comparing lorlatinib to crizotinib in the first-line treatment of patients with metastatic ALK-positive NSCLC.

Lorlatinib is an investigational agent and has not received regulatory approval for any indication anywhere in the world.

About Dacomitinib

Dacomitinib is an investigational, second-generation, oral, once-daily, irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. It has not received regulatory approval anywhere in the world.

About XALKORI (crizotinib)

XALKORI is a tyrosine kinase inhibitor indicated in the U.S. for the treatment of patients with metastatic non-small cell lung cancer (NSCLC) whose tumors are anaplastic lymphoma kinase (ALK) or ROS1-positive as detected by an FDA-approved test. XALKORI has received approval for patients with ALK-positive NSCLC in more than 90 countries, including Australia, Canada, China, Japan, South Korea and the European Union.

XALKORI Important Safety Information

Hepatotoxicity: Drug-induced hepatotoxicity with fatal outcome occurred in 0.1% of patients treated with XALKORI across clinical trials (n=1719). Transaminase elevations generally occurred within the first 2 months. Monitor liver function tests, including ALT, AST, and total bilirubin, every 2 weeks during the first 2 months of treatment, then once a month, and as clinically indicated, with more frequent repeat testing for increased liver transaminases, alkaline phosphatase, or total bilirubin in patients who develop transaminase elevations. Permanently discontinue for ALT/AST elevation >3 times ULN with concurrent total bilirubin elevation >1.5 times ULN (in the absence of cholestasis or hemolysis); otherwise, temporarily suspend and dose-reduce XALKORI as indicated.

Interstitial Lung Disease (Pneumonitis): Severe, life-threatening, or fatal interstitial lung disease (ILD)/pneumonitis can occur. Across clinical trials (n=1719), 2.9% of XALKORI-treated patients had any grade ILD, 1.0% had Grade 3/4, and 0.5% had fatal ILD. ILD generally occurred within 3 months after initiation of treatment. Monitor for pulmonary symptoms indicative of ILD/pneumonitis. Exclude other potential causes and permanently discontinue XALKORI in patients with drug-related ILD/pneumonitis.

QT Interval Prolongation: QTc prolongation can occur. Across clinical trials (n=1616), 2.1% of patients had QTcF (corrected QT by the Fridericia method) 500 ms and 5.0% had an increase from baseline QTcF 60 ms by automated machine-read evaluation of ECGs. Avoid use in patients with congenital long QT syndrome. Monitor ECGs and electrolytes in patients with congestive heart failure, bradyarrhythmias, electrolyte abnormalities, or who are taking medications that prolong the QT interval. Permanently discontinue XALKORI in patients who develop QTc >500 ms or 60 ms change from baseline with Torsade de pointes, polymorphic ventricular tachycardia, or signs/symptoms of serious arrhythmia. Withhold XALKORI in patients who develop QTc >500 ms on at least 2 separate ECGs until recovery to a QTc -480 ms, then resume at a reduced dose.

Bradycardia: Symptomatic bradycardia can occur. Across clinical trials, bradycardia occurred in 12.7% of patients treated with XALKORI (n=1719). Avoid use in combination with other agents known to cause bradycardia. Monitor heart rate and blood pressure regularly. In cases of symptomatic bradycardia that is not life-threatening, hold XALKORI until recovery to asymptomatic bradycardia or to a heart rate of 60 bpm, re-evaluate the use of concomitant medications, and adjust the dose of XALKORI. Permanently discontinue for life-threatening bradycardia due to XALKORI; however, if associated with concomitant medications known to cause bradycardia or hypotension, hold XALKORI until recovery to asymptomatic bradycardia or to a heart rate of 60 bpm. If concomitant medications can be adjusted or discontinued, restart XALKORI at 250 mg once daily with frequent monitoring.

Severe Visual Loss: Across clinical trials, the incidence of Grade 4 visual field defect with vision loss was 0.2% (n=1719). Discontinue XALKORI in patients with new onset of severe visual loss (best corrected vision less than 20/200 in one or both eyes). Perform an ophthalmological evaluation. There is insufficient information to characterize the risks of resumption of XALKORI in patients with a severe visual loss; a decision to resume should consider the potential benefits to the patient.

Vision Disorders: Most commonly visual impairment, photopsia, blurred vision or vitreous floaters, occurred in 63.1% of 1719 patients. The majority (95%) of these patients had Grade 1 visual adverse reactions. 0.8% of patients had Grade 3 and 0.2% had Grade 4 visual impairment. The majority of patients on the XALKORI arms in Studies 1 and 2 (>50%) reported visual disturbances which occurred at a frequency of 4-7 days each week, lasted up to 1 minute, and had mild or no impact on daily activities.

Embryo-Fetal Toxicity: XALKORI can cause fetal harm when administered to a pregnant woman. Advise of the potential risk to the fetus. Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment and for at least 45 days (females) or 90 days (males) respectively, following the final dose of XALKORI.

ROS1-positive Metastatic NSCLC: Safety was evaluated in 50 patients with ROS1-positive metastatic NSCLC from a single-arm study, and was generally consistent with the safety profile of XALKORI evaluated in patients with ALK-positive metastatic NSCLC. Vision disorders occurred in 92% of patients in the ROS1 study; 90% of patients had Grade 1 vision disorders and 2% had Grade 2.

Adverse Reactions: Safety was evaluated in a phase 3 study in previously untreated patients with ALK-positive metastatic NSCLC randomized to XALKORI (n=171) or chemotherapy (n=169). Serious adverse events were reported in 34% of patients treated with XALKORI, the most frequent were dyspnea (4.1%) and pulmonary embolism (2.9%). Fatal adverse events in XALKORI-treated patients occurred in 2.3% of patients, consisting of septic shock, acute respiratory failure, and diabetic ketoacidosis. Common adverse reactions (all grades) occurring in ≥25% and more commonly (≥5%) in patients treated with XALKORI vs chemotherapy were vision disorder (71% vs 10%), diarrhea (61% vs 13%), edema (49% vs 12%), vomiting (46% vs 36%), constipation (43% vs 30%), upper respiratory infection (32% vs 12%), dysgeusia (26% vs 5%), and abdominal pain (26% vs 12%). Grade 3/4 reactions occurring at a ≥2% higher incidence with XALKORI vs chemotherapy were QT prolongation (2% vs 0%), esophagitis (2% vs 0%), and constipation (2% vs 0%). In patients treated with XALKORI vs chemotherapy, the following occurred: elevation of ALT (any grade [79% vs 33%] or Grade 3/4 [15% vs 2%]); elevation of AST (any grade [66% vs 28%] or Grade 3/4 [8% vs 1%]); neutropenia (any grade [52% vs 59%] or Grade 3/4 [11% vs 16%]); lymphopenia (any grade [48% vs 53%] or Grade 3/4 [7% vs 13%]); hypophosphatemia (any grade [32% vs 21%] or Grade 3/4 [10% vs 6%]). In patients treated with XALKORI vs chemotherapy, renal cysts occurred (5% vs 1%). Nausea (56%), decreased appetite (30%), fatigue (29%), and neuropathy (21%) also occurred in patients taking XALKORI.

Drug Interactions: Exercise caution with concomitant use of moderate CYP3A inhibitors. Avoid grapefruit or grapefruit juice which may increase plasma concentrations of crizotinib. Avoid concomitant use of strong CYP3A inducers and inhibitors. Avoid concomitant use of CYP3A substrates with narrow therapeutic range in patients taking XALKORI. If concomitant use of CYP3A substrates with narrow therapeutic range is required in patients taking XALKORI, dose reductions of the CYP3A substrates may be required due to adverse reactions.

Lactation: Because of the potential for adverse reactions in breastfed infants, advise females not to breastfeed during treatment with XALKORI and for 45 days after the final dose.

Hepatic Impairment: XALKORI has not been studied in patients with hepatic impairment. As crizotinib is extensively metabolized in the liver, hepatic impairment is likely to increase plasma crizotinib concentrations. Use caution in patients with hepatic impairment.

Renal Impairment: Decreases in estimated glomerular filtration rate occurred in patients treated with XALKORI. Administer XALKORI at a starting dose of 250 mg taken orally once daily in patients with severe renal impairment (CLcr <30 mL/min) not requiring dialysis. No starting dose adjustment is needed for patients with mild and moderate renal impairment. For more information and full prescribing information, please visit www.XALKORI.com.

ZIOPHARM Oncology Announces First Patient Dosed in New Phase 1 Study of Ad-RTS-hIL-12 plus Veledimex for the Treatment of Pediatric Brain Tumors

On October 16, 2017 ZIOPHARM Oncology, Inc. (Nasdaq:ZIOP), a biopharmaceutical company developing new gene and cell-based immunotherapies for cancer, reported that the first patient has been dosed in a new Phase 1 study of Ad-RTS-hIL-12 with veledimex for the treatment of pediatric brain tumors (Press release, Ziopharm, OCT 16, 2017, View Source [SID1234520948]).

This open label study will assess the safety and tolerability of a single intratumoral injection of Ad-RTS-hIL-12, a gene therapy designed to control the expression of human interleukin 12 (hIL-12), a critical protein for stimulating a localized anti-cancer immune response. The study is conducted in two groups: the first is comprised of pediatric patients with recurrent or progressive brain tumors in the cortex, while the second is comprised of pediatric patients with diffuse intrinsic pontine glioma (DIPG).

“Studies in adults with recurrent glioblastoma have shown that Ad-RTS-hIL-12 with veledimex is not only well tolerated, but also have shown growing evidence that this treatment elicits a targeted immune response against brain tumor cells that gives rise to improvement in overall survival,” said Francois Lebel, M.D., Executive Vice President, Research and Development, Chief Medical Officer at ZIOPHARM. “We look forward to advancing our studies in pediatric patients with brain tumors as these patients have limited-to-no therapeutic options.”

This Phase 1 study is being conducted at leading pediatric cancer centers across the United States, including Ann & Robert H. Lurie Children’s Hospital in Chicago, Dana-Farber Cancer Institute in Boston and the University of California, San Francisco. The first pediatric patient to receive Ad-RTS-hIL-12 plus veledimex is receiving care at Lurie Children’s.

“Pediatric gliomas are a devastating diagnosis for children and families, and DIPG, specifically, while rare, is extremely aggressive and always a fatal disease with no viable treatment options,” said Stewart Goldman, M.D., Division Head Hematology-Oncology, Neuro-Oncology & Stem Cell Transplantation at Lurie Children’s. “We look forward to evaluating the potential of Ad-RTS-hIL-12 plus veledimex as a treatment option for children with brain tumors.”

About Glioma

Glioblastoma (GBM) is a fast-growing, aggressive type of central nervous system tumor, with an estimated 12,390 new adult cases predicted in 2017 according to the American Brain Tumor Association. Recurrence rates for this type of cancer are near 90 percent, and prognosis for adult patients is poor with treatment often combining multiple approaches including surgery, radiation and chemotherapy i. In children, the incidence of brain cancer is approximately 4.84 per 100,000, according to the National Cancer Institute. Glioma in the cortex (cerebrum) of children is unusual and is treated along the same lines as in adults with occurrence common and survival poor. Glioma in the pontine region of the brain, or DIPG, accounts for approximately 15 percent of all cases of pediatric brain tumors, with a median survival time of less than one yearii. Because of where these tumors are situated, DIPG is inaccessible to surgery and there are no curative options.

About Ad-RTS-hIL-12 plus Veledimex

ZIOPHARM is advancing Ad-RTS-hIL-12 plus veledimex as a gene therapy for recurrent GBM (rGBM). Ad-RTS-hIL-12 is an adenoviral vector administered via a single injection into the tumor and engineered to express hIL-12, a powerful cytokine that has demonstrated the potential to stimulate a targeted, anti-tumor immune response. The expression of hIL-12 is controlled and modulated with the RheoSwitch Therapeutic System (RTS) by the small molecule veledimex, an activator ligand which has been shown to cross the blood brain barrier. The Company has recently reported that biopsies from three patients treated with Ad-RTS-hIL-12 plus veledimex provided evidence of documented pseudo-progression rather than tumor progression. Pseudo-progression may be seen in serial post-treatment imaging studies of cancers where the tumor appears larger compared to baseline, but these changes are due to infiltration of immune cells, as evidenced by subsequent biopsies. ZIOPHARM’s Phase 1 stereotactic study of Ad-RTS-hIL-12 with veledimex for the treatment of patients with brain tumors is underway. The Company also plans to initiate enrollment of adult patients with rGBM who will receive a single dose of Ad-RTS-hIL-12 plus veledimex in combination with a checkpoint inhibitor targeting programmed cell death protein 1 (PD-1) by the end of the year.

6-K – Report of foreign issuer [Rules 13a-16 and 15d-16]

On October 16, 2017 Trillium Therapeutics Inc. (NASDAQ/TSX: TRIL), a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, reported that new preclinical data and a patient case study for its CD47-blocking agent, TTI-621 (SIRPa-IgG1 Fc), were presented at the EORTC CLTF meeting “Cutaneous Lymphomas – Insights and Therapeutic Progress”, October 13-15, in London, England (Press release, Trillium Therapeutics, OCT 16, 2017, View Source [SID1234520947]).

Oral Presentation O-16: CD47 Blockade with TTI-621 (SIRPαFc) in Sézary Syndrome
Presenter: Dr. Oleg Akilov, University of Pittsburgh

This oral presentation highlighted that leukemic cells from patients with Sézary syndrome, a form of cutaneous T cell lymphoma (CTCL), express the CD47 “do not eat” signal at almost four times the level of normal lymphocytes and that over-expression of CD47 is associated with poor prognosis. In vitro experiments demonstrated that blockade of CD47, employing TTI-621, may constitute a promising therapeutic approach for patients with Sézary syndrome. Two clinical trials of TTI-621 that include patients with relapsed or refractory CTCL are ongoing at multiple North American sites (NCT02663518 and NCT02890368).

Poster Presentation P-10: Synergistic Effect of Successive Administration of TTI-621 (SIRPαFc) and PEGylated Interferon-α2a in a Patient with Sézary Syndrome
Presenter: Dr. Oleg Akilov, University of Pittsburgh

This case study reported local and systemic anti-tumor activity in a Sézary syndrome patient treated with a single intratumoral dose of TTI-621. Administration of PEGylated Interferon-α2a seven days after TTI-621 resulted in decreased leukemic burden and improvements in clinical symptoms. Trillium believes such a reduction is not observed regularly with standard regimens and would not be anticipated following PEGylated Interferon-α2a monotherapy, suggesting a synergistic effect of TTI-621 and PEGylated Interferon-α2a.

“CTCL patients are being treated in both our intratumoral and intravenous trials,” said Dr. Niclas Stiernholm, Trillium’s Chief Executive Officer. “Careful study of the effects of TTI-621 in CTCL patients potentially provides us with a unique opportunity to better understand the mechanism behind TTI-621’s anti-tumor activity and the role of CD47 in the overall immuno-oncology landscape, ultimately leading to targeted indications and combination therapies with sound scientific rationale.”

About Cutaneous T-Cell Lymphoma (CTCL)

CTCL is a rare type of non-Hodgkin’s lymphoma which is characterized by localization of malignant T lymphocytes to the skin. The two most common types of CTCL are mycosis fungoides and Sézary syndrome. The disease most often involves the skin, may progress to involve lymph nodes, blood, viscera and other organs, and in select cases may become leukemic.

Kura Oncology Announces Late-Breaking Presentations for Tipifarnib in HRAS Mutant Squamous Head and Neck Cancer and for KO-539 in AML at Upcoming AACR-NCI-EORTC International Conference

On October 16, 2017 Kura Oncology, Inc. (Nasdaq:KURA), a clinical stage biopharmaceutical company focused on the development of precision medicines for oncology, reported presentations at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper), taking place October 26-30, 2017 in Philadelphia (Press release, Kura Oncology, OCT 16, 2017, View Source;p=RssLanding&cat=news&id=2308717 [SID1234520946]).

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!

A late-breaking poster will be presented on Saturday, October 28, by Dr. Alan Ho of Memorial Sloan Kettering Cancer Center and will feature data from Kura’s recently-announced positive Phase 2 proof-of-concept trial in head and neck squamous cell carcinoma (HNSCC) with HRAS mutations. In addition, the poster has been selected as the subject of a short, oral presentation during the Spotlight on Proffered Papers Session 1 on Friday, October 27.

A second late-breaking poster will be presented on Saturday, October 28, and will feature preclinical data for KO-539, Kura’s potent and selective inhibitor of the menin-MLL interaction, supporting the potential clinical utility of KO-539 in NPM1- and DNMT3A-mutant AML.

The schedule and locations for the late-breaking oral presentation and poster presentations is as follows:

Oral Presentation:

Title of Presentation: Preliminary results from a Phase 2 proof-of-concept trial of tipifarnib in tumors with HRAS mutations
Date & Time: Friday, October 27, 2017, 10:50 a.m. – 12:20 p.m. EDT
Presenter: Alan L. Ho, M.D., Ph.D., Memorial Sloan Kettering Cancer Center
Session: Spotlight on Proffered Papers Session 1
Location: Terrace Ballroom, 400 Level, Pennsylvania Convention Center

Poster Presentations:

Title of Poster: Preliminary results from a Phase 2 proof-of-concept trial of tipifarnib in tumors with HRAS mutations
Date & Time: Saturday, October 28, 12:30 p.m. – 4:00 p.m. EDT
Presenter: Alan L. Ho, M.D., Ph.D., Memorial Sloan Kettering Cancer Center
Session: Late-Breaking Poster Session A (Clinical Trials)
Abstract Number: LB-A10
Location: Hall E, Pennsylvania Convention Center

Title of Poster: A novel small molecule menin-MLL inhibitor for potential treatment of MLL-rearranged leukemias and NPM1/DNMT3A-mutant AML
Date & Time: Saturday, October 28, 12:30 p.m. – 4:00 p.m. EDT
Presenter: Francis Burrows, Ph.D., Kura Oncology
Late-Breaking Poster Session A (Epigenetic Targets)
Abstract Number: LB-A27
Location: Hall E, Pennsylvania Convention Center