Cancer Research UK, The Lustgarten foundation and Stand Up To Cancer join forces in £8 million pancreatic cancer venture

On November 6, 2015 Cancer Research UK reported that it, The Lustgarten Foundation (link is external), and Stand Up To Cancer have come together in an international collaboration worth £8 million ($12 million) to announce funding for a pancreatic cancer research ‘Dream Team’ (Press release, Cancer Research UK, NOV 6, 2015, View Source [SID:1234508074]).

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"These are among the finest researchers in the world and we’re really excited by the potential of their ideas in the fight against this terrible disease" – Dr Iain Foulkes, Cancer Research UK

This innovative funding approach, into a cancer with low survival rates and in urgent need of better treatments, will support over 24 researchers across the UK and US over the next three years.

This transatlantic ‘Dream Team’ of top researchers will tackle the toughest questions in pancreatic cancer. The initiative will research new ways to turn off faulty molecular switches in pancreatic cancer cells, which control the behaviour of a wide range of genes that can play a part in the development of the disease.

Ultimately the research aims to increase the effectiveness of chemotherapy and harness the power of the patient’s own immune system, leading to new ways to prevent pancreatic cancer from returning after initial treatment.

Professor Gerard Evan, Cancer Research UK’s co-leader of the ‘Dream Team’ and cancer gene expert at the University of Cambridge (link is external), said: "Despite the apparent diversity in pancreatic cancer, there are remarkable similarities in the biological pathways behind pancreatic tumours. Our goal is to exploit these to identify common targets for the development of more accurate and effective treatments for patients affected by this awful disease."

Around 8,500 in the UK and an estimated 40,000 people in the US will die from pancreatic cancer this year. The disease is the seventh leading cause of cancer death worldwide.

Professor Daniel Von Hoff, director of translational research at the Translational Genomics Research Institute (link is external), Arizona, who is leading the research team, said: "We’re going after pancreatic cancer in a different way. We will use new and existing drugs to reprogramme the master regulatory biological machinery in cancer cells that drives tumour growth. This machinery comprises molecular complexes of DNA and proteins that are known as ‘super enhancers’ for their ability to coordinate the expression of a large number of genes.

"By resetting the malfunctioning genome in both pancreatic tumour cells as well as the surrounding non-cancer cells on which the cancer cells rely for support, the team will try to increase the sensitivity of tumours to chemotherapy and make them vulnerable to the patient’s immune response."

Kerri Kaplan, executive director and chief operating officer of The Lustgarten Foundation, said: "To eradicate pancreatic cancer will take a collaborative effort and private funding plays a critical role in accelerating the development of new clinical trials for this deadly disease. This international collaboration will bring together leading global experts in the field of pancreatic cancer research, and together, we will focus on developing new therapies and innovative approaches so patients can benefit and live longer lives."

Dr Iain Foulkes, Cancer Research UK’s executive director of research funding, said: "Survival from pancreatic cancer is low – only three percent of patients in the UK survive their disease for five years or more. Frankly, progress has not been good enough and it’s why we have invested nearly £4 million in this ‘Dream Team’. These are among the finest researchers in the world and we’re really excited by the potential of their ideas in the fight against this terrible disease."

Preclinical Studies Find That Tarloxotinib May Overcome Resistance to EGFR Tyrosine Kinase Inhibitors

On November 6, 2015 Threshold Pharmaceuticals, Inc. (NASDAQ: THLD) reported new preclinical data demonstrating that tarloxotinib bromide*, or tarloxotinib, may overcome resistance to first- and second- and third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) (Press release, Threshold Pharmaceuticals, NOV 6, 2015, View Source [SID:1234508073]). The data will be reported today in two scientific posters (Abstracts A66 and A67) at the AACR (Free AACR Whitepaper)-NCI-EORTC Molecular Targets and Cancer Therapeutics Meeting being held November 5-9, 2015, Boston. Tarloxotinib is Threshold’s proprietary hypoxia-activated prodrug of an irreversible EGFR TKI exclusively licensed from the University of Auckland, New Zealand.

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The research to be reported at the meeting focuses on preclinical models of EGFR-dependent cancers including non-small cell lung cancer (NSCLC) and squamous cell carcinomas of the head and neck (SCCHN) or skin (SCCS). These types of cancers are currently treated with drugs that block the activity of EGFR to interfere with tumor cell growth, but most tumors ultimately become resistant to therapy, and some do not respond at all.

Scientists are trying to understand the mechanisms underlying EGFR inhibitor resistance and discover new treatment options for patients with EGFR-driven cancers.

At the meeting, Adam Patterson, Ph.D. and Jeff Smaill, Ph.D., of the University of Auckland, New Zealand, will report that switching to low-dose tarloxotinib treatment in laboratory models of NSCLC resulted in significant regression of tumors that were progressing despite ongoing treatment with erlotinib, a first-generation EGFR TKI. These tumor models were heterozygous for EGFR whereby both wild-type (normal) and mutant (abnormal) forms of EGFR were present.

Independent research has shown that persistent wild-type EGFR signaling is associated with TKI resistance1, and patients with heterozygous EGFR-mutant NSCLC have worse outcomes following EGFR TKI therapy than those with pure mutant-EGFR disease2.

"Our research supports the hypothesis that persistent wild-type EGFR signaling within the tumor may be an important yet underappreciated mechanism of resistance to TKIs," Patterson said.

To test for the role of wild-type EGFR signaling in TKI resistance, Patterson and colleagues engineered one NSCLC model to have extra copies of the gene for wild-type EGFR. In the original parental heterozygous model, treatment with osimertinib (AZD9291), a third-generation TKI designed to "spare" wild-type EGFR, led to tumor regressions. In contrast, in the genetically engineered model with about 40% more wild-type EGFR, tumors started to regrow after initially responding to osimertinib. Tumor regrowth was brought under control upon switching to tarloxotinib treatment, which resulted in immediate and marked tumor regressions.

"Our preliminary findings suggest that tarloxotinib may be able to overcome wild-type EGFR-driven resistance to TKI therapy," Patterson said. "We believe this is related to the role of hypoxia in driving wild-type EGFR signaling within tumors coupled with the hypoxia-activation of tarloxotinib."

Using special imaging techniques, the team led by Patterson and Smaill were able to show a spatial overlap between hypoxic regions within tumors and EGFR signaling. Similarly, they were able to visualize the areas within a tumor where tarloxotinib released its TKI and found these areas to comprise the hypoxic compartment.

"Through collaboration with Dr. Angus Grey from the University of Auckland, we have for the first time demonstrated the mechanism of action of a hypoxia-activated prodrug in a human tumor model using MALDI Imaging Mass Spectrometry. This promises to be a very important technique for this field moving forward," Patterson said.

The scientists also presented data on tarloxotinib in models of SCCHN and SCCS. Across multiple cancer in vitro cell lines, tarloxotinib’s TKI exhibited greater anti-proliferative activity and consistently silenced EGFR signaling to a greater extent than equimolar concentrations of cetuximab, afatinib or dacomitinib. When tested in in vivo models, tarloxotinib was more effective compared to afatinib in controlling SCCS tumor growth, and compared to cetuximab in controlling SCCHN tumor growth. A single dose of tarloxotinib significantly reduced the hypoxic compartment in a SCCHN tumor model.

"Taken all together, the data suggest that preferential activation of tarloxotinib in the hypoxic tumor microenvironment leads to reduction of the hypoxic compartment and effective silencing of EGFR signaling within the tumor," Smaill said. "Tumor-targeted activation of tarloxotinib may limit systemic side effects, and wild-type EGFR shut down may address an apparently important mechanism of TKI resistance, both potentially contributing to better outcomes for patients with EGFR-dependent cancers."

"This important translational work continues to support our ongoing proof-of-concept Phase 2 trials in patients with NSCLC and in patients with SCCHN and SCCS," said Tillman Pearce, MD, Chief Medical Officer at Threshold. "Initial PET imaging using our proprietary hypoxia imaging agent, [18F]-HX4, shows that imaging hypoxia in these tumors is possible. We hope that by combining imaging with response data we can start to determine which patients would benefit most from tarloxotinib therapy. We look forward to having preliminary results from these studies in the first half of 2016."

About Non-Small Cell Lung Cancer

Lung cancer is the most common cause of death from cancer worldwide; an estimated 1.8 million new cases were diagnosed in 20123. The most common type of lung cancer, non-small cell lung cancer (NSCLC), accounts for approximately 85 to 90 percent of cases4. EGFR activating mutations occur in approximately 10 percent of NSCLC cases in Caucasian patients and up to 35 percent in Asian patients5. Tarceva, Iressa, and Gilotrif are the first- and second-generation EGFR inhibitors currently approved for patients with the EGFR activating mutations. Nearly all patients ultimately progress on these therapies due to a variety of resistance mechanisms.

About Squamous Cell Carcinomas Head and Neck

Most head and neck cancers, which include cancers of the larynx (voice box), throat, lips, mouth, nose, and salivary glands, begin in the squamous cells that line the moist surfaces inside the head and neck, and are therefore referred to as squamous cell carcinomas of the head and neck (SCCHN). SCCHN is diagnosed in approximately 59,000 people in the U.S. annually and is responsible for some 12,000 deaths6. In the recurrent/metastatic setting, chemotherapy or cetuximab monotherapy is the standard of care with response rates are about ten percent and disease progression occurs within two to three months.7

About Squamous Cell Carcinomas of the Skin

Non-melanoma skin cancers typically resulting from chronic sun exposure or other sources of ultraviolet rays are the most common types of cancer. Twenty percent of these skin cancers originate from squamous cells normally present in the outer layers of the skin (SCCS); five percent of SCCS will become locally advanced, recur, or metastasize. In the U.S., approximately 2,000 deaths per year are attributed to SCCS8. As with SCCHN, SCCS is associated with EGFR overexpression and appear to be responsive to EGFR inhibitor therapy9.

About Tarloxotinib Bromide

Tarloxotinib bromide, or "tarloxotinib," is a prodrug designed to selectively release a covalent (irreversible) EGFR tyrosine kinase inhibitor under severe hypoxia, a feature of many solid tumors. Accordingly, tarloxotinib has the potential to effectively shut down aberrant EGFR signaling in a tumor-selective manner, thus potentially avoiding or reducing the systemic side effects associated with currently available EGFR tyrosine kinase inhibitors. Tarloxotinib is currently being evaluated in two Phase 2 proof-of-concept trials: one for the treatment of patients with mutant EGFR-positive, T790M-negative advanced non-small cell lung cancer progressing on an EGFR tyrosine kinase inhibitor, and the other for patients with recurrent or metastatic squamous cell carcinomas of the head and neck or skin. Threshold licensed exclusive worldwide rights to tarloxotinib from the University of Auckland, New Zealand, in September 2014.

About [18F]-HX4

[18F]-HX4 [flortanidazole (18F)] is a novel investigational tumor hypoxia tracer developed to potentially identify and quantify the degree of hypoxia in tumors in vivo. Positron emission tomography (PET) is a nuclear medical imaging technique that non-invasively produces a three-dimensional image of functional processes in the entire body. PET is routinely used to inform physicians on diagnosis and treatment of cancer and is used in cancer treatment centers globally. [18F]HX4 has a 2-nitroimidazole "trigger" that is designed to be activated under the extreme hypoxic conditions generally found in tumors but not typically in normal healthy tissue. Clinical data has demonstrated the potential of [18F]HX4 to quantify the degree of hypoxia within different tumors.

8-K – Current report

On November 6, 2015 Stemline Therapeutics, Inc. (Nasdaq:STML) reported financial results for the quarter ended September 30, 2015 (Filing, 8-K, Stemline Therapeutics, NOV 6, 2015, View Source [SID:1234508072]).

Ivan Bergstein, M.D., Stemline’s Chief Executive Officer, commented, "During the third quarter, we made significant progress on many fronts as we continue to advance our clinical programs forward. We are actively enrolling patients, and opening additional sites, in the expansion stage of our ongoing SL-401 pivotal trial in blastic plasmacytoid dendritic cell neoplasm, BPDCN. We look forward to sharing clinical updates from both the lead-in and initial expansion stages of this trial at the upcoming American Society of Hematology (ASH) (Free ASH Whitepaper) meeting this December, and on into next year."

Dr. Bergstein continued, "We remain focused on the BPDCN indication while continuing to pursue expansion opportunities for SL-401 in additional malignancies. We have single agent trials currently open in several indications and we anticipate combination studies coming on-line as well. We are also continuing to develop our other pipeline candidates, SL-701 and SL-801, and look forward to treating our first patient with SL-801, our novel XPO1 inhibitor, early next year. With a strong cash position and multiple ongoing programs advancing across a range of indications of unmet medical need, we remain focused on achieving our objective of building a leading commercial stage biopharmaceutical company."

Third Quarter 2015 Financial Results Review

Stemline ended the third quarter of 2015 with $104.0 million in cash, cash equivalents and investments, as compared to $58.6 million as of December 31, 2014. In the first quarter of 2015, the Company completed an equity offering raising $68.6 million in gross cash proceeds on the sale of 4.4 million common shares.

For the third quarter of 2015, Stemline had a net loss of $9.2 million, or $0.53 per share, compared with a net loss of $6.9 million, or $0.53 per share, for the same period in 2014.

Research and development expenses were $7.3 million for the third quarter of 2015, which reflects an increase of $2.3 million compared with $5.0 million for the third quarter of 2014. The higher expenses during the third quarter were primarily attributable to the ramp up of SL-401 and SL-701 clinical activities. Also, we incurred costs relating to SL-801 IND-enabling studies.

General and administrative expenses were $2.2 million for the third quarter of 2015, which reflects an increase of $0.2 million compared with $2.0 million for the third quarter of 2014. The higher costs were primarily attributable to an increase in non-cash stock based compensation expense relating to employees.

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PharmaMar presents clinical studies for YONDELIS® (trabectedin) during the international congress CTOS

On November 6, 2015 PharmaMar (MSE:PHM) reported that the Company will showcase several clinical studies with YONDELIS (trabectedin) in soft tissue sarcoma (STS) during the 20th anniversary CTOS (Connective Tissue Oncology Society) meeting that will be held in Salt Lake City, Utah, from the 4-7 November, 2015 (Press release, PharmaMar, NOV 6, 2015, View Source [SID:1234508070]). This forum will gather oncologist experts and investigators to share new results and experiences to move forward basic and applied research on connective tissue-related cancers.

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In addition to presenting several studies for YONDELIS (trabectedin) in STS, PharmaMar has organized a stand-alone meeting in which Javier Martín Broto, MD, President of the Spanish Sarcoma Research Group and Peter Reichardt, MD, Professor and Head of the Hematology and Oncology Department, Sarcoma Center HELIOS Klinikum Bad Saarow, Germany, have discussed the clinical development story of YONDELIS in STS.

During his presentation, Dr. Martín Broto has showcased the pivotal studies that led to the approval in the European Union and the U.S., the clinical trial STS-201 and the SAR-3007ii, respectively. To date, approximately 50.000 pacientes have been treated with YONDELIS worldwide. The expert has pointed out how everything started with the authorization of commercialization of YONDELIS for soft tissue sarcoma by the European Commission, resulting in the first anticancer drug of marine origin.

Trabectedin, an effective therapy in second line treatment

Trabectedin is an anticancer drug that has shown to decrease tumor density and to induce tumor shrinkage, two clinical measurements that should be considered in patients treated with this drug when assessing tumor responseiii. "Understanding
how to correctly define tumor progression in patients treated with trabectedin is important for the decision making strategy to prevent interruption of a treatment that may provide clinical benefit after 6 cycles of treatment, in some cases" added Dr. Martín Broto. This is one of the main points that were concluded from the clinical trials carried out by the French sarcoma Group in 2015, which include the large retrospective study called Retrospectyon, and the prospective trial T-DIS. The oncologist Dr. Martín Broto added that "when patients continued receiving trabectedin until disease progression, instead of stopping the treatment after 6
cycles, the next disease relapse is delayed."

Since 2003 when the first clinical study started until now, trabectedin has demonstrated that it is the treatment of choice for pacients with STS treated in the second-line setting as "this drug provides prolonged survival, has an optimal safety profile, has received approval for all subtypes of STS and it is currently included in the ESMO (Free ESMO Whitepaper) Clinical Guidelines and very soon will be also in the NCCN Clinical Practice Guidelines".

Main studies presented at CTOS

 Y-IMAGE study: a non-interventional, prospective phase IV study of trabectedin in patients with advanced soft tissue sarcoma (STS). Main author: Penel et al.

 Efficacy and safety of trabectedin as an early treatment for advanced STS: an interim analysis of a non-interventional, prospective Phase IV study. Main author: Mazzeo et al.

 Trabectedin in elderly patients with recurrent soft tissue sarcoma (STS): an interim analysis of a non-interventional, prospective Phase IV study. Main author: Buonadonna et al.

 Final results of two phase II studies, a randomized comparative study and a single arm study, of trabectedin in patients (PTS) with translocation-related sarcomas (TRS) – patrocinado por Taiho Pharmaceuticals. Main author: Kawai, A et al.

 Single-center experience of high-grade chondrosarcoma treated with trabectedin – patrocinado por Janssen Research & Development, LLC. Main author: Chawla.

 Final Overall Survival (OS) Analysis of the Randomized Phase 3 Study of Trabectedin (T) or Dacarbazine (D) for the Treatment of
Patients (pts) with Advanced Leiomyosarcoma (LMS) or Liposarcoma (LPS) – patrocinado por Janssen Research & Development, LLC. Main author: Shreyaskumar R. Patel, Margaret von Mehren, Damon.

 Efficacy and Safety of Trabectedin (T) or Dacarbazine (D) in an Elderly Patient subgroup (+65 years) with Advanced Leiomyosarcoma (LMS) or Liposarcoma (LPS) after Prior Chemotherapy – patrocinado por Janssen Research & Development, LLC. Main author: Margaret von Mehren, George D. Demetri, Scott M Sc

 Efficacy and Safety of Trabectedin(T) or Dacarbazine (D) for Treatment of Patients (pts) with Advanced Leiomyosarcoma (LMS)
or Liposarcoma (LPS) after Prior Chemotherapy – patrocinado por Janssen Research & Development, LLC. Main author: George D.
Demetri, Shreyaskumar R. Patel, Samuel Th

 Trabectedin in patient with an abdominal small round cells desmoplastic tumour: a case report. Main author: J. Casanova, P.
Tavares, R. Ferreira

 Analysis of trabectedin safety in teenage young adults with STS. Cambridge University Hospital-Addrnbrookes

About YONDELIS (trabectedin)

YONDELIS (trabectedin) is a novel, multimodal, synthetically produced antitumor agent, originally derived from the sea squirt, Ecteinascidia turbinata. The drug exerts its activity by targeting the transcriptional machinery and impairing DNA repair. It is approved in 80 countries in North America, Europe, South America and Asia for the treatment of advanced soft tissue sarcomas as a single-agent and for relapsed ovarian cancer in combination with DOXIL/CAELYX (doxorubicin HCl liposome injection). Under a licensing agreement with PharmaMar, Janssen Products, L.P. has the rights to develop and sell YONDELIS globally except in Europe, where PharmaMar holds the rights, and in Japan, where PharmaMar has granted a license to Taiho Pharmaceuticals.

About Soft Tissue Sarcoma

Soft tissue sarcoma is a type of cancer originating in the soft tissues that connect, support and surround other body structures, such as muscle, fat, blood vessels, nerves, tendons and the lining of jointsiv,v. In the United States, nearly 12,000 people will be diagnosed and approximately 4,870 are expected to die of soft tissue sarcomas in 2015.

Idera Pharmaceuticals Reports Third Quarter 2015 Financial Results and Provides Corporate Update

On November 06, 2015 Idera Pharmaceuticals, Inc. (NASDAQ:IDRA), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel nucleic acid-based therapeutics for oncology and rare diseases, reported its financial and operational results for the third quarter ended September 30, 2015 (Press release, Idera Pharmaceuticals, NOV 6, 2015, View Source;p=RssLanding&cat=news&id=2107923 [SID:1234508068]).

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"We’ve made a great deal of progress at Idera through the first three quarters of 2015, which sets up our company for a number of important catalysts in this last quarter of the year," stated Vincent Milano, Idera’s Chief Executive Officer. "As we announced yesterday, we will be presenting the clinical and safety data analysis from our Phase 1/2 clinical trial of IMO-8400 in Waldenström’s macroglobulinemia at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in December. We also are initiating our clinical studies of our TLR9 agonist, IMO-2125 in combination with ipilmumab in patients with metastatic melanoma and IMO-8400 Phase 2 study in dermatomyositis, this quarter. Finally, as detailed in the following text, we are today announcing the first two gene targets for our third generation antisense technology platform."

Continued Milano, "I’m very pleased with the progress that our team at Idera has made over the past months and quarters as we’ve integrated the existing Idera team with many new contributors all the while maintaining the rigor and momentum to ensure our company is positioned for both near and long-term success."

Research and Development Program Updates

IMO-8400 and IMO-2125 are our lead clinical development drug candidates. IMO-8400 is an oligonucleotide-based antagonist of Toll-like receptors (TLRs) 7, 8, and 9. IMO-2125 is an oligonucleotide-based agonist of TLR9.

Toll-like Receptor (TLR) Agonism Program

Immuno-Oncology Program

In June 2015, the company announced that it had entered into a strategic clinical research alliance with MD Anderson Cancer Center to advance the clinical development of intra-tumoral TLR9 agonists in combination with checkpoint inhibitors. The company also announced that it expects to initiate the first trial from the alliance, a Phase 1/2 study to assess the safety and efficacy of intra-tumoral IMO-2125 in combination with ipilimumab in approximately 45 patients with metastatic melanoma. The company is on track to initiate this study in the fourth quarter of 2015. Planning of additional studies as part of the clinical research alliance with MD Anderson Cancer Center is in progress. Additionally, the company presented new preclinical data demonstrating the combination of IMO-2125 and PD1 in cancer models 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) on November 5th in Boston, MA.

Toll-like Receptor (TLR) Antagonism Programs

Genetically Defined Forms of B-cell Lymphoma

Idera’s program in genetically defined forms of B-cell lymphoma is based on pre-clinical studies that have demonstrated, in certain B-cell lymphomas that the presence of the MYD88 L265P oncogenic mutation led to over-activation of TLR7 and TLR9 signaling and that blocking these TLRs with our antagonists promoted tumor cell death.

In the company’s Phase 1/2 study in Waldenstrom’s macroglobulinemia, the targeted number of patients at each of the three dose levels completed assessment through the end of their first cycle of treatment; the dose escalation portion of the study has also been completed. The trial is designed to evaluate IMO-8400’s safety, tolerability and potential clinical activity in patients who have a history of relapse after or failure to respond to prior therapies. Idera announced yesterday that data from this Phase 1/2 clinical study will be presented as a poster at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting on Saturday, December 5th from 5:30 PM ET – 7:30 PM ET.

During the third quarter the company also continued to enroll patients into the first of three dose cohorts of our Phase 1/2 clinical trial of IMO-8400 in patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) who are harboring the MYD88 L265P oncogenic mutation. The company currently anticipates that data from this trial will become available in 2016.

Idera previously announced that the U.S. Food and Drug Administration (FDA) granted us orphan drug designation for IMO-8400 for the treatment of Waldenström’s macroglobulinemia and DLBCL.

Rare Disease Programs

The company is planning to initiate clinical development of IMO-8400 for the treatment of rare autoimmune and autoinflammatory diseases. The company has selected dermatomyositis and Duchenne muscular dystrophy (DMD) as the first rare diseases for which we plan to develop IMO-8400. The company selected these indications for development based on the reported increase in TLR expression in these disease states, expression of cytokines indicative of key TLR-mediated pathways, the identification of prospective biomarkers for evaluation in early clinical trials and significant unmet needs. The company plans to progress clinical development in these two indications by initiating a Phase 2 clinical trial in dermatomyositis in the fourth quarter of 2015 and a Phase 2 clinical trial in DMD in 2016.

Third Generation Antisense Platform

Throughout 2015, the company undertook an analysis and prioritization of oncology and rare disease indications for potential development of drug candidates derived from our third generation antisense technology platform. The key considerations in identifying disease indications from our third generation antisense program included: strong evidence that the disease is caused by a specific protein; clear criteria to identify a target patient population; biomarkers for early assessment of clinical proof-of-concept; a targeted therapeutic mechanism for action; and unmet medical need to allow for a well-defined development path to approval and commercial opportunity. As a result of this analysis, the company has selected NLRP3 (NOD-like receptor family, pyrin domain containing protein 3) and DUX4 (Double Homeobox 4) as gene targets to advance into IND-enabling activities, which will occur throughout 2016. Potential disease indications include, but are not limited to interstitial cystitis, uveitis and facioscapulohumeral muscular dystrophy (FSHD), respectively. The company intends to describe these programs in more detail during the 2016 JP Morgan Healthcare Conference early next year.

Financial Results

Third Quarter 2015 Results
Net loss applicable to common stockholders for the three months ended September 30, 2015 was $11.4 million, or $ (0.10) per diluted share, compared to a net loss applicable to common stockholders of $9.6 million, or $ (0.11) per diluted share, for the same period in 2014. For the nine month period ended September 30, 2015, the Company’s net loss applicable to common stockholders was $36.6 million, or $ (0.32) per diluted share, compared to a net loss applicable to common stockholders of $27.1 million, or $ (0.33) per diluted share, for the same period in 2014. The company recognized nominal revenue in the third quarter and nine month periods of 2015 and 2014.

Research and development expenses for the three months ended September 30, 2015 totaled $7.5 million compared to $6.7 million for the same period in 2014. For the nine month period ended September 30, 2015, research and development expenses totaled $25.1 million compared to $19.2 million for the same period in 2014.

General and administrative expenses for the three months ended September 30, 2015 totaled $4.0 million compared to $2.9 million for the same period in 2014. For the nine month period ended September 30, 2015, general and administrative expenses totaled $11.7 million compared to $7.6 million for the same period in 2014.

As of September 30, 2015, Idera’s cash, cash equivalents and investments totaled $94.7 million compared to $48.6 million as of December 31, 2014.