On March 28, 2017 Aptose Biosciences Inc. (NASDAQ:APTO) (TSX:APS), a clinical-stage company developing highly differentiated therapeutics that target the underlying mechanisms of cancer, reported financial results for the three months and fiscal year ended December 31, 2016 and reported on corporate developments (Press release, Aptose Biosciences, MAR 28, 2017, View Source [SID1234518291]). Unless specified otherwise, all amounts are in Canadian dollars.

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The net loss for the year ended December 31, 2016 was $18.6 million ($1.46 per share) compared with $14.6 million ($1.23 per share) in the year ended December 31, 2015. Total cash and cash equivalents and investments as of December 31, 2016 were $10.7 million (or $7.9 million US Dollars).
"We began 2017 by reviewing our corporate strategy and refocusing our resources on CG’806, an oral first-in-class pan-FLT3/BTK inhibitor we are developing for patients with FLT3-driven AML and certain B-cell malignancies," said William G. Rice, Ph.D., Chairman, President and Chief Executive Officer. "Preclinical studies with CG‘806 have demonstrated a unique activity profile which warranted the prioritization of resources toward advancing its development. We look forward to reporting on our progress with this molecule."
Corporate Highlights
In January 2017, Aptose announced the prioritization of its resources toward the development of CG’806, an oral preclinical compound being developed for patients with FLT3-driven acute myeloid leukemia (AML) and certain BTK-driven B-cell malignancies.

In June 2016, Aptose entered into an exclusive global option and license agreement with CrystalGenomics, Inc. of South Korea, focused on the development of CG’806. Aptose is currently conducting Investigational New Drug (IND) enabling studies, and, if it exercises its option under the agreement, expects to initiate a Phase 1 clinical trial in early 2018. The potential option exercise would likely occur prior to submission of an IND application in the U.S. Upon exercise of the option, Aptose would own global rights to develop and commercialize the program outside of Korea and China.

Compelling preclinical data have established CG’806 as a potent and well-differentiated pan-FLT3 inhibitor for AML and a non-covalent inhibitor of BTK and other oncogenic kinases that drive certain B-cell derived cancer cells. The compound has demonstrated tumor elimination in the absence of toxicity in AML xenograft models.

Aptose recently developed a new synthetic route to synthesize greater amounts of CG’806, and is using that route to prepare drug substance for various preclinical and animal model studies, and for development of an improved oral formulation. The compound is being developed as a once-daily oral therapeutic.

The company has submitted research abstracts to present CG’806 data at the upcoming AACR (Free AACR Whitepaper)-Hematologic Malignancies Meeting in May 2017.

Aptose temporarily delayed clinical activities with APTO-253, a phase 1 stage compound for AML, in an effort to define the root cause of recent manufacturing setbacks related to the intravenous formulation, and to restore the molecule to a state supporting clinical development and potential partnering. Aptose remains hopeful in the viability of APTO-253, which effectively inhibits expression of the c-Myc oncogene, as a potential treatment for AML.
Financial Results
THREE MONTHS ENDED DECEMBER 31, 2016 AND 2015 (UNAUDITED)
(Amounts in 000’s except for per common
share data) Dec 31,
2016
Dec 31,
2015
Revenue $ ― $ ―
Research and development expense 2,550 2,340
General and administrative expense 1,461 2,364
Operating expenses 4,011 4,794
Finance expense − −
Finance income (85 ) (273 )
Net financing income (85 ) (273 )
Net loss 3,926 (4,431 )
Basic and diluted net loss per share $ (0.26 ) $ (0.38 )

Aptose’s net loss for the three months ended December 31, 2016 was $3.9 million ($0.26 per share) compared with $4.4 million ($0.38 per share) in the same period in the prior year.
Research and development costs increased to $2.6 million in the three months ended December 31, 2016 compared with $2.3 million for the three months ended December 2015. Aptose incurred higher costs for formulation studies and manufacturing costs for the APTO-253 product in the three months ended December 31, 2016 than in the comparable period, and these were offset by lower expenses for the contract research organization costs to manage the study. In addition, in the current period Aptose was conducting studies related to its CG’806 program following the licensing of the technology in June 2016.
General and administrative expenses decreased to $1.5 million in the three months ended December 31, 2016 compared with $2.4 million in the three months ended December 31, 2015. The decrease, despite the increased cost of Aptose’s US dollar expenditures due to the devaluation of the Canadian dollar, is related to lower stock option compensation and lower consulting fees related to projects that were active and completed in the fourth quarter in 2015.
FULL YEAR RESULTS

Year ended Year ended
(amounts in 000’s of Canadian Dollars except for per common share data) Dec. 31, 2016 Dec. 31, 2015
REVENUE $ - $
-
EXPENSES
Research and development 10,322 6,254
General and administrative 8,344 9,845
Operating expenses 18,666 16,099
Finance expense 66 43
Finance income (105 ) (1,556 )
Net financing (income) expense (39 ) (1,473 )
Net loss and comprehensive loss for the period 18,627 14,626
Basic and diluted loss per common share $ 1.46 $ 1.23

Weighted average number of common shares 12,743 11,906

RESEARCH AND DEVELOPMENT
Research and development expenses totaled $10.3 million in the year ended December 31, 2016 compared with $6.3 million in the year ended December 31, 2015. Research and development costs consist of the following:
Year ended
December 31,
2016 Year ended
December 31,
2015

Research and Development excluding salaries $ 6,442 $ 4,046
CrystalGenomics Option Fee 1,294 -
Salaries 2,246 1,969
Stock-based compensation 293 210
Depreciation of equipment 47 29
$ 10,322 $ 6,254

Expenditures for the year ended December 31, 2016 increased significantly over the year ended December 31, 2015 due to the following reasons:
Research and development activities related to the option fee for CG’806;
Costs associated with the LALS/Moffitt collaboration developing epigenetic single molecule inhibitors of multiple targets, including the BET proteins, and other kinases for which no comparable expenses existed in the prior year periods;
Increased research and clinical operations headcount and related costs;
Formulation and manufacturing costs associated with APTO-253 and the root cause analysis of the filter clogging identified in November 2015; and
Increased Contract Research Organization costs related to consultants and advisors as we worked towards returning APTO-253 to the clinic.
During the year ended December 31, 2016, Aptose paid US$1.0 million ($1.294 million) to CrystalGenomics for an option fee related to the CG’806 technology. Should Aptose elect to exercise the option prior to filing of an IND application with the FDA, we would pay an additional US$2.0 million in cash or combination of cash and common shares, and would receive full development and commercial rights for the program in all territories outside of Korea and China. No comparable expense existed in the same period in the prior year.
GENERAL AND ADMINISTRATIVE
General and administrative expenses totaled $8.3 million in the year ended December 31, 2016 compared to $9.8 million in the year ended December 31, 2015. General and administrative expenses consisted of the following:
Year ended
December 31,
2016 Year ended
December 31,
2015

General and administrative excluding salaries $ 3,412 $ 4,317
Salaries 3,095 2,859
Stock-based compensation 1,730 2,602
Depreciation of equipment 107 67
$ 8,344 $ 9,845

General and administrative expenses excluding salaries, decreased in the year ended December 31, 2016 compared with the year ended December 31, 2015. The decrease is the result of lower travel, consulting and legal costs in the current year related to transactions completed in the prior year as well as lower press release and filing costs associated with a lower cost service provider in the current year periods.
Salary charges in the year ended December 31, 2016 increased in comparison with the year ended December 31, 2015 due to additional headcount in the first half of 2016 compared with the first half of 2015 as well as a higher average CA/US exchange rate which increased the cost of Aptose’s US denominated salaries in the first six months of 2016 in comparison with the prior year, and higher bonus expenses recognized in the current period.
Stock-based compensation decreased in the year ended December 31, 2016 compared with the year ended December 31, 2015 due to large option grants in April, June and July 2014 which vested 50% during the first year and therefore contribute to higher stock-based compensation expense during the first twelve month period captured in the prior year period.
FINANCE INCOME
Finance income totaled $105 thousand in the year ended December 31, 2016 compared to $1.5 million in the year ended December 31, 2015.
Interest income represents interest earned on Aptose’s cash and cash equivalent and investment balances. Foreign exchange gains are the result of an increase in the value of US dollar denominated cash and cash equivalents balances during such periods due to a depreciation of the Canadian dollar compared to the US dollar.

On March 28, 2017 Compugen Ltd. (NASDAQ: CGEN), a therapeutic discovery company, reported the selection of COM902 as the lead clinical antibody candidate for its CGEN-15137/TIGIT T cell checkpoint inhibitor program in immuno-oncology (Press release, Compugen, MAR 28, 2017, View Source [SID1234518290]). COM902 follows COM701 into the Company’s preclinical development pipeline. COM701 is the Company’s lead therapeutic antibody targeting PVRIG, for which IND is anticipated later this year. As previously disclosed, PVRIG and TIGIT represent two distinct but complementary arms of the same biological pathway, and inhibition of the two results in increased activation of tumor infiltrating lymphocytes (TILs). This provides a strong clinical rationale for the combination of COM701 and COM902, in addition to monotherapy use, as immunotherapies to treat various cancer types.

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Anat Cohen-Dayag, PhD, CEO and President of Compugen, commented, "The addition of this lead clinical antibody candidate for CGEN-15137/TIGIT to our preclinical pipeline represents another important milestone as we continue to build toward becoming a clinical stage company. We began our TIGIT program in 2016 based on our data indicating the potential for enhanced efficacy for combination treatment with COM701, and with our prior finding that TIGIT and PVRIG operate in the same biological pathway. The knowledge and the expertise we gained through the development of COM701 were an important factor in the accelerated development and selection of COM902. COM902 is a high affinity antagonist antibody selected for its potential ability to activate immune responses, both alone and in combination with COM701."

Dr. Cohen-Dayag added, "Currently available immuno-oncology therapies are effective for only a select subset of cancer patients, and we believe that the combination of COM701 and COM902, as well as with other checkpoint inhibitors, could provide a new therapeutic venue for treating cancer patients, specifically those non-responsive to current therapies. As we continue our development toward the clinic, we look forward to sharing with you more data as it becomes available."

About TIGIT
TIGIT is an immune checkpoint in the B7/CD28 family which has recently gained broad industry interest in the field of immuno-oncology. TIGIT was discovered by Compugen utilizing its in silico predictive discovery infrastructure and experimentally validated as an immune checkpoint. These findings were published by Compugen in the October 2009 issue of the Proceedings of National Academy of Sciences (PNAS). In the same year, two other groups also published papers disclosing TIGIT as a new checkpoint. Antibodies targeting TIGIT being developed by others entered Phase I clinical studies in 2016.

TIGIT can inhibit both T cell and NK cell activation when bound to its ligand, PVR (also known as CD155). TIGIT expression is increased on tumor infiltrating lymphocytes (TILs), and inhibition of T cell activation by TIGIT has been reported to be mediated by its ability to disrupt DNAM-1 (also known as CD226) costimulatory signals. Recent preclinical studies have shown that antibody antagonists of TIGIT can potently inhibit tumor growth in mouse cancer models when combined with PD-1 pathway blockade.

On March 28, 2017 DelMar Pharmaceuticals (Nasdaq: DMPI) ("DelMar" and the "Company"), a biopharmaceutical company focused on the development and commercialization of new cancer therapies, reported that it will present three abstracts at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (Press release, DelMar Pharmaceuticals, MAR 28, 2017, View Source [SID1234518289]). The abstracts are based on research conducted with DelMar’s lead anti-cancer product candidate, VAL-083 (dianhydrogalactitol), a "first-in-class" small-molecule DNA-targeting agent. The AACR (Free AACR Whitepaper) Annual Meeting will be held April 1-5, 2017 in Washington, D.C.

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Details of the poster presentations by DelMar and/or its collaborators are as follows:

Abstract #1429 – DNA damage response to dianhydrogalactitol (VAL-083) in p53-deficient non-small cell lung cancer cells
Section: Genomic Instability and Cancer Therapy
Date and Time: Monday, April 3, 2017, 8:00 a.m. – 12:00 p.m. Eastern Time

Abstract #2483 – Molecular mechanisms of dianhydrogalactitol (VAL-083) in overcoming chemoresistance in glioblastoma
Section: Homologous Recombination and DNA Double-Strand Break Repair
Date and Time: Monday, April 3, 2017, 1:00 p.m. – 5:00 p.m. Eastern Time

Abstract CT#054 – Phase II study of dianhydrogalactitol in patients with MGMT-unmethylated bevacizumab-naive recurrent glioblastoma
Section: Phase III Clinical Trials and Phase II/III Clinical Trials in Progress
Date and Time: Monday, April 3, 2017, 1:00 p.m. – 5:00 p.m. Eastern Time

The Company’s first two abstracts have been published and can be viewed on the AACR (Free AACR Whitepaper) Annual Meeting website.

About VAL-083
VAL-083 is a "first-in-class," small-molecule DNA-targeting agent that demonstrated clinical activity against a range of cancers including GBM in historical clinical trials sponsored by the U.S. National Cancer Institute. DelMar has demonstrated that VAL-083’s anti-tumor activity against GBM is unaffected by the expression of MGMT in vitro. Further details can be found at www.delmarpharma.com/scientific-publications.html.

VAL-083 has received an orphan drug designation in Europe for the treatment of malignant gliomas, and the U.S. FDA Office of Orphan Products has granted an orphan designation to VAL-083 for the treatment of glioma, medulloblastoma and ovarian cancer.

DelMar has also announced plans to advance VAL-083 into a pivotal randomized multi-center Phase 3 clinical trial for the treatment of bevacizumab-failed GBM. A separate Phase 2 trial for MGMT-unmethylated recurrent GBM is currently open for enrollment at the University of Texas MD Anderson Cancer Center and an international trial for newly diagnosed MGMT-unmethylated GBM is expected to commence enrollment upon receipt of required government approval.

DelMar believes that data from its clinical trials, if successful, will form the basis of a new treatment paradigm for the vast majority of GBM patients whose tumors exhibit features that make them unlikely to respond to currently available therapies.

About Glioblastoma Multiforme (GBM)
GBM is the most common as well as the most lethal form of brain cancer. Approximately 15,000 new cases of GBM are expected to be diagnosed in the United States during 2017. GBM progresses quickly and patients deteriorate rapidly. Common symptoms include headaches, seizures, nausea, weakness, paralysis and personality or cognitive changes such as loss of speech or difficulty in thinking clearly. The majority of GBM patients do not survive for more than two years following diagnosis, and the median survival in newly diagnosed patients with best available treatments is less than 15 months.

On March 28, 2017 AstraZeneca, along with its global biologics research and development arm, MedImmune, reported it will present the strength and depth of its translational science, which is expected to deliver the Company’s next wave of innovative oncology medicines, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Washington DC, US, 1-5 April 2017 (Press release, AstraZeneca, MAR 28, 2017, View Source [SID1234518288]).

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In addition to demonstrating a robust early oncology portfolio in DNA Damage Response (DDR) and Tumour Drivers and Resistance, AstraZeneca will highlight the continued progress being made in early Immuno-Oncology (IO) and Antibody-Drug Conjugate (ADC) science.

Susan Galbraith, Senior Vice President, Head of Oncology, Innovative Medicines and Early Development (IMED) Biotech Unit, said: "The progress we will report at AACR (Free AACR Whitepaper) 2017 highlights the rapid growth of our highly-differentiated DNA Damage Response portfolio that targets a broad range of key molecular pathways. Presentations will also show our progress within Tumour Drivers and Resistance with the development of molecules targeting two key mechanisms that tumours use to resist cell death, namely MCL-1 and CDK9."

David Berman, Senior Vice President, Head of Oncology Innovative Medicines at MedImmune, added: "AACR 2017 is an exciting moment for our next-generation oncology portfolio, demonstrating how our broad biologics pipeline is targeting the multiple ways cancer evades the immune system. We will update on our scientific progress in cancer Immuno-Oncology, including predictive biomarkers of response to immune checkpoint inhibitors. We also look forward to presenting the first clinical trial results for our TLR 7/8 agonist, an important mechanism for immunologically-silent tumours, and to sharing updates from our Antibody-Drug Conjugate platform, a key pillar of AstraZeneca’s oncology strategy."

Shedding new light on Tumour Drivers and Resistance

AstraZeneca was a pioneer in the development of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) for patients with non-small cell lung cancer (NSCLC) (Iressa, Tagrisso), and continues to work on the unmet needs of patients who fail to respond, or respond for limited periods, to these compounds. An expanding programme of tumour cell-death research is targeting upregulation of key proteins that cancer cells use to evade death, including myeloid cell leukaemia 1 (MCL-1) and cyclin-dependent kinase 9 (CDK9) and is leveraging the sophistication of macrocyles – larger, cyclic compounds – to address the complexity of protein interactions.

Presentations include:

AZD4205, a potent inhibitor of Janus kinase 1 (JAK1), part of the JAK1/signal transducer and activator of transcription (STAT) axis, which is understood to play an important role in tumour escape from EGFR-targeted treatment (oral presentation; Abstract #979)
The first preclinical data presented on AZD5991 demonstrating the tumour cell-killing potential of this potent, selective macrocylic inhibitor of MCL-1 in blood cancers (oral presentation; Abstract #DDT01)
AZD4205 combined with Tagrisso (osimertinib) in patients with EGFR mutation-positive NSCLC to reduce residual tumour burden and prolong the benefit of osimertinib (Abstract #4046)
Preclinical data supporting the potential of the CDK9 inhibitor, AZD5576, alone and in combination with AstraZeneca’s potentially best-in-class Bruton’s tyrosine kinase (BTK) inhibitor, acalabrutinib, in the treatment of non-Hodgkin lymphoma (Abstract #4295).
A leading DNA Damage Response (DDR) position

With one approved medicine and four candidates in clinical development, AstraZeneca is extending its leadership in medicines that target novel DDR deficiencies to selectively kill cancer cells, while minimising the impact on normal cells.

Four oral presentations will include the following data:

Phase I/II studies exploring the combination of Lynparza (olaparib) and temozolomide (an alkylating chemotherapy) in patients with small-cell lung cancer (SCLC) following failure of prior chemotherapy (Abstract #CT048), and
A Phase I study of Lynparza and the alpha-specific PI3-kinase inhibitor BYL719, in patients with recurrent ovarian and breast cancer (Abstract #CT008)
Preclinical data uncovering a novel role for the bromodomain protein, BRD4, in regulating DNA replication-stress response, and the potential of the combination of the BRD4 inhibitor, AZD5153, and the ATR inhibitor, AZD6738, in the sustained delay of tumour growth (Abstract #1026)
The European paediatric precision medicine programme in recurrent tumours showing first results from the MAPPYACTS molecular profiling trial aimed at increasing the number of targetable genomic alternations for DDR therapies (Abstract #CT004)
Preliminary results will also be reported from a Phase I dose-escalation study of the ataxia-telangiectasia and Rad3 related (ATR) inhibitor, AZD6738, in advanced solid tumours (PATRIOT Part A) (Abstract #CT084).

Immuno-Oncology (IO): Activating the immune system via multiple approaches

Presentations will illustrate the depth of AstraZeneca’s IO capabilities beyond its comprehensive late-stage portfolio.

Key presentations include:

Oral presentation of innovative computer modelling to identify tumour and immune cell interactions during disease progression to predict susceptibility to checkpoint inhibitors and other compounds (Abstract #975)
Phase I data on the Toll-like receptor 7/8 (TLR7/8) agonist MEDI9197 in solid tumours (Abstract #CT091) and preclinical data showing its anti-tumour activity in combination with PD-L1 or CTLA-4 checkpoint inhibitors (Abstract #4697)
Phase I/II data showing that high pre-treatment levels of interferon gamma gene signature are associated with greater benefit with durvalumab in patients with NSCLC and urothelial bladder cancer (Abstract #1773).
Antibody-Drug Conjugates: Sophisticated targeting of toxic payloads

AstraZeneca will share data demonstrating the potential of a range of ADCs in targeting cytotoxic treatments to tumour cells. These include preclinical data with toxic pyrrolobenzodiazepine (PBD) or tubulysin payloads in combination with multiple immunotherapies (Abstract #4596), and data on the potent anti-tumour activity of ADCT-401/MEDI3726 when targeting prostate-specific membrane antigen (PSMA) in prostate cancer models (Abstract #3111A).

On March 28, 2017 AbbVie, a global biopharmaceutical company, and M2Gen, a leading health informatics solutions company, reported that AbbVie has joined the Oncology Research Information Exchange Network (ORIEN) Avatar Research Program (Press release, AbbVie, MAR 28, 2017, View Source [SID1234518286]). Launched in April of 2016, the ORIEN Avatar Research Program fosters collaboration among key stakeholders in cancer research with the shared goal of discovering and developing novel therapies in clinical trials.

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ORIEN Avatar is a collaboration between the 15 leading U.S. cancer hospitals that comprise ORIEN, leading pharmaceutical companies and M2Gen, which manages the program. AbbVie is the fourth pharmaceutical company to participate in the Avatar Program.

The ORIEN Avatar Research Program was borne out of the ORIEN Cancer Initiative, which launched in 2014. A first-of-its-kind effort in cancer research, ORIEN joins leading cancer centers across the U.S. to better study the disease and encourage collaboration in research and development across nearly 20 types of cancer. ORIEN Avatar’s current focus areas have the potential to affect more than 1.4 million newly diagnosed patients in the U.S. annually. Patients at participating ORIEN hospitals donate clinical and molecular data through their consent to the Total Cancer Care (TCC) Protocol, building a wealth of data that includes more than 150,000 patients to date.

The Avatar Program represents an unprecedented, pre-competitive approach to fighting cancer. Cancer researchers contribute samples and disease information from patients who have consented to the Total Cancer Care Protocol. This provides rich molecular data that helps identify eligible participants for clinical trials. Pharmaceutical companies contribute financial support, and both companies and ORIEN member institutions receive access to de-identified genetic and disease information that can be used to inform the discovery and clinical development of novel cancer therapeutics. By matching the right patient to the right trial, ORIEN Avatar helps to accelerate the discovery and development of novel therapies for millions of patients.

"The ORIEN Avatar Research Program offers a unique and important opportunity in the effort to develop new treatments and cures for cancer," said Steve Davidsen, Vice President, Oncology Discovery, AbbVie. "We see enormous potential to improve patient recruitment and targeting for clinical trials, especially more in specific subsets of patients. Through the collaborative efforts of the ORIEN Avatar participants, we can magnify the collective data on specific tumor types and biomarkers to catalyze future discoveries for patients in need."

"We are pleased to welcome AbbVie to the ORIEN Avatar Research Program, and inspired by their commitment, to oncology research and development," said William Dalton, PhD, MD, founder and CEO of M2Gen. "This program offers the opportunity to make great strides in how we treat cancer. AbbVie is a partner that clearly understands the potential of ORIEN Avatar; that common understanding and passion for the work will only further enable our success for cancer patients."