On November 10, 2015 DelMar Pharmaceuticals, Inc. (OTCQX: DMPI) ("DelMar" and the "Company"), a biopharmaceutical company focused on the development and commercialization of new cancer therapies, reported the presentation by its collaborators from the University of British Columbia (UBC) and Vancouver Prostate Centre (VPC) of additional data on the unique molecular signaling events responsible for VAL-083 (dianhydrogalactitol) activity against cancer (Press release, DelMar Pharmaceuticals, NOV 10, 2015, View Source [SID:1234508180]).

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"We continue to demonstrate the therapeutic potential of VAL-083 both as a single-agent and in combination with other treatments," stated Jeffrey Bacha, DelMar’s president and CEO. "We have previously shown that VAL-083’s anti-tumor activity is unaffected by the expression of MGMT, a DNA repair enzyme that is implicated in chemotherapy resistance. To further understand the unique anti-cancer mechanism of VAL-083, we collaborated with researchers from UBC and VPC to study VAL-083’s anti-cancer activity on a molecular level."

These new data were presented on November 9th by UBC and VPC researchers in a poster entitled, "Exploring the Molecular Mechanisms of Dianhydrogalactitol (VAL-083) in Cancer Treatment," at the 2015 Canadian Cancer Research Conference of the Canadian Cancer Research Alliance (CCRA).

"The study results show a pattern of durability in the DNA lesions caused by VAL-083 which indicate its unique mechanism and potential superiority versus other chemotherapeutic agents. This suggests that VAL-083 is effective at modifying tumor cells and may halt tumor progression by inhibiting natural cellular repair processes," added Mr. Bacha.

"VAL-083’s broad anti-cancer activity was established in prior clinical trials sponsored by the U.S. National Cancer Institutes (NCI). Employing modern biological tools to differentiate the mechanisms involved in VAL-083’s anti-cancer activity from other chemotherapies provides a basis for future combination treatments as well as guidance for our drug development efforts to concentrate on tumor-types representing significant unmet medical needs," Mr. Bacha stated.

VAL-083 is a bi-functional alkylating agent causing N7-guanine methylation and interstrand DNA crosslinks and is approved in China as a chemotherapeutic drug for the treatment of chronic myelogenous leukemia and lung cancer. Preclinical studies and clinical trial data suggest that VAL-083 may be active against a range of tumor types via a novel mechanism of action that could provide improved treatment options for patients.

The goal of this study was to further understand the detailed molecular mechanisms mediating VAL-083 sensitivity or resistance in cancer by investigating the signaling events responsible for VAL-083 activity against cancer. The study confirmed a four-fold hypotheses:

VAL-083 induces DNA double-strand breaks (DSBs).

VAL-083 cytotoxicity is due to cell cycle arrest and apoptosis resulting from DNA cross-linking lesions accumulating in S- and G2-phases of the cell cycle.
The antineoplastic effect of VAL-083 is dependent on cancer cells’ ability to repair the VAL-083-induced DNA damage.
Alterations in DNA damage repair signaling pathway lead to VAL-083 sensitivity or resistance in tumor cells.
Results indicate that treatment of cancer cells by VAL-083 induces phosphorylation of H2AX, a hallmark of double-strand DNA breaks. H2AX is a histone involved in the CHK2 checkpoint activation pathway, a key component of the body’s immune response to DNA damage resulting in down-stream signaling ultimately resulting in apoptosis.

"We will continue to explore the signaling pathways involved in VAL-083 for the treatment of cancer," added Mr. Bacha. "The further elucidation of these molecular mechanisms will help to focus our drug development efforts on patients with cancer who would most benefit from VAL-083 treatment. This ‘personalized-medicine’ approach leverages significant historical clinical data from prior NCI-sponsored studies; which, when juxtaposed against new understanding of VAL-083’s biological mechanism, provides an opportunity to accelerate the development of VAL-083 as a new therapy for cancer patients with limited treatment options."

The research presented at the 2015 Cancer Research Conference was funded in part by financial contributions from Canada’s National Research Council’s Industrial Research Assistance Program (NRC-IRAP) and Mitacs, a Canadian Network of Centres of Excellence, dedicated to supporting scientific and industrial research.

The poster on the molecular mechanisms of VAL-083 may be found on DelMar’s website under View Source

About VAL-083

VAL-083 is a "first-in-class," small-molecule chemotherapeutic. In more than 40 Phase I and II clinical studies sponsored by the U.S. National Cancer Institute, VAL-083 demonstrated clinical activity against a range of cancers including lung, brain, cervical, ovarian tumors and leukemia both as a single-agent and in combination with other treatments. VAL-083 is approved in China for the treatment of chronic myelogenous leukemia (CML) and lung cancer, and has received orphan drug designation in Europe and the U.S. for the treatment of malignant gliomas.

DelMar has demonstrated that VAL-083’s anti-tumor activity is unaffected by the expression of MGMT, a DNA repair enzyme that is implicated in chemotherapy resistance and poor outcomes in GBM patients following standard front-line treatment with Temodar (temozolomide).

DelMar recently announced the completion of enrollment in a Phase II clinical trial of VAL-083 in refractory GBM. Patients have been enrolled at five clinical centers in the United States: Mayo Clinic (Rochester, MN); UCSF (San Francisco, CA) and three centers associated with the Sarah Cannon Cancer Research Institute (Nashville, TN, Sarasota, FL and Denver, CO).

In the Phase I dose-escalation portion of the study, VAL-083 was well tolerated at doses up to 40mg/m2 using a regimen of daily x 3 every 21 days. Adverse events were typically mild to moderate; no treatment-related serious adverse events reported at doses up to 40 mg/m2. Dose limiting toxicity (DLT) defined by thrombocytopenia (low platelet counts) was observed in two of six (33%) of patients at 50 mg/m2. Generally, DLT-related symptoms resolved rapidly and spontaneously without concomitant treatment, although one patient who presented with hemorrhoids received a platelet transfusion as a precautionary measure.

Sub-group analysis of data from the Phase I dose-escalation portion of the study suggested a dose-dependent and clinically meaningful survival benefit following treatment with VAL-083 in GBM patients whose tumors had progressed following standard treatment with temozolomide, radiotherapy, bevacizumab and a range of salvage therapies.

Patients in a low dose (≤5mg/m2) sub-group had a median survival of approximately five (5) months versus median survival of approximately nine (9) months for patients in the therapeutic dose (30mg/m2 & 40mg/m2) sub-group following initiation of VAL-083 treatment. DelMar reported increased survival at 6, 9 and 12 months following initiation of treatment with VAL-083 in the therapeutic dose sub-group compared to the low dose sub-group.

On November 10, 2015 Celator Pharmaceuticals, Inc. (Nasdaq: CPXX) reported the presentation of positive results from its CombiPlex technology platform applied to drug combinations incorporating molecularly targeted agents (MTAs) 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) (Press release, Celator Pharmaceuticals, NOV 10, 2015, View Source [SID:1234508179]).

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CombiPlex is Celator’s proprietary technology that uses nano-scale drug carriers to ensure the optimal ratio of anticancer drugs are simultaneously delivered and selectively exposed to tumor cells for prolonged periods of time while reducing drug exposure and toxicity to normal tissues. The technology addresses difficulties often experienced with conventional MTA combination regimens, where significant toxicities and/or incomplete target inhibition can lead to sub-optimal patient outcomes.

Pre-clinical data presented at the conference demonstrated the broad applicability of Celator’s hydrophobic prodrug nanoparticle (HPN) delivery technology to MTAs from diverse classes, including inhibitors of MEK, Akt, HSP90, B-Raf and FGFR. In all cases, Celator’s proprietary HPN delivery eliminated the early drug distribution phase observed for conventional formulations of these agents, which historically has been associated with significant exposure and toxicity to normal tissues. In fact, HPN co-formulated combinations of docetaxel plus the HSP90 inhibitor AUY922, and the MEK:Akt inhibitor combination of selumetinib plus ipatasertib, could be administered at much higher drug exposure with maintained improvements in safety while also resulting in increased efficacy.

The largest improvements were observed in tumor models known to be more resistant to conventional dosing forms of the two combinations. Optimal efficacy was achieved at drug ratios of 1:2 and 2:1, respectively. In the case of docetaxel:AUY922, the conventional formulation provided negligible tumor growth delay at the maximum tolerated dose (MTD) in the OVCAR-8 human ovarian xenograft model with tumors reaching 1 gram in size in approximately 25 days. In contrast, dosing with Celator’s proprietary HPN formulation at MTD, tumors grew to only half that size after 50 days demonstrating potent tumor growth inhibition.

"As an oncologist who has personally experienced the challenges with combining conventional formulations of molecularly targeted agents in a clinical setting, I am very encouraged by the results Celator has generated using its CombiPlex technology," said Dr. Tony Tolcher, director of clinical research at South Texas Accelerated Research Therapeutics. "This approach could provide an important breakthrough in our ability to optimize the therapeutic index and patient outcomes for many molecularly targeted agent combinations."

Once HPN formulation conditions were optimized for these initial combinations, the approach was readily extended to the B-Raf inhibitor GDC0879 and the FGFR inhibitor LY2874455 and both were successfully co-formulated with the MEK inhibitor selumetinib resulting in coordinated drug exposure in the plasma. In addition, the drug components could be "mixed and matched," and this versatility was then taken one step further by generating a 3-drug combination, co-formulating selumetinib, AUY922 and docetaxel into a single HPN that exhibited a plasma half-life in the range of 10 hours in mice with no early distribution phase.

"The CombiPlex technology platform continues to deliver on its promise to optimize the efficacy of a wide range of anticancer drug combinations," said Dr. Lawrence Mayer, president and chief scientific officer at Celator. "The successful application of this technology to molecularly targeted agents across a wide range of drug classes makes a compelling data package that we believe will be instrumental in attracting R&D collaborations with pharmaceutical companies."

On November 10, 2015 Aptose Biosciences Inc. (Nasdaq:APTO) (TSX:APS), a clinical-stage company developing new therapeutics and molecular diagnostics that target the underlying mechanisms of cancer, reported two collaborations that will provide exclusive access to new epigenetic therapeutics for the Company’s oncology pipeline (Filing, 6-K, Aptose Biosciences, NOV 10, 2015, View Source [SID:1234508178]). These partnerships have been strategically formed to leverage Aptose’s scientific and clinical expertise in cancer and hematologic diseases to develop mechanistically differentiated and high-value epigenetic drug candidates.

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Strategic Collaboration with Moffitt Cancer Center

Aptose has entered into a definitive agreement with Moffitt Cancer Center for exclusive global rights to potent, multi-targeting, single-agent inhibitors for the treatment of hematologic and solid tumor cancers. These small molecule agents are highly differentiated inhibitors of the Bromodomain and Extra-Terminal motif (BET) protein family members, which simultaneously target specific kinase enzymes. The molecules developed by Moffitt exhibit single-digit nanomolar potency against the BET family members and specific oncogenic kinases which, when inhibited, are synergistic with BET inhibition. Under the agreement, Aptose will gain access to the drug candidates developed by Moffitt and the underlying intellectual property covering the chemical modifications enabling potent bromodomain (BRD) inhibition on the chemical backbone of a kinase inhibitor. Aptose expects lead clinical candidates to emerge from the collaboration by late 2016.

Transcriptional dysregulation in cancer cells may occur through various means, including chromatin remodeling, histone modification and super-enhancer formation. The bromodomain proteins play a critical role in this dysregulation, and hence targeting specific bromodomains represents a validated treatment approach for various cancers. Aptose is committed to developing a pipeline of molecules that inhibit key epigenetic targets with the potential to intervene in oncogenesis and induce remission.

"We’ve built an oncology drug development organization with valuable ties to leading clinical centers and thought leaders," said William G. Rice, Ph.D., Chairman, President and CEO, "and we are exceptionally pleased to partner with Moffitt on advancing new epigenetic inhibitors, specifically bromodomain inhibitors that simultaneously inhibit specific kinases in key regulatory pathways."

"Aptose views a multi-targeting approach, which incorporates bromodomain inhibition, as an exciting means to enhance efficacy and diminish therapeutic resistance relative to the current landscape in cancer treatment. This is even more beneficial when inhibition of the pathways is highly synergistic. The researchers at Moffitt have made unprecedented progress in this field," continued Dr. Rice.

"We view the advancement of epigenetic multi-inhibitors as a highly promising strategy in the treatment of cancer," said the principal investigators Ernst Schonbrunn, Ph.D. and Nicholas Lawrence, Ph.D., members of the Drug Discovery Program at Moffitt, "and targeting broad-acting epigenetic regulators of transcription like bromodomain proteins is needed to suppress the induction of gene expression that results when cancer cells respond to kinase inhibitors."

"We are excited to work with an organization as scientifically driven to develop novel therapeutics as Aptose," said Haskell Adler, Ph.D., MBA, Senior Licensing Manager at Moffitt.

Exclusive Agreement with Laxai Avanti Life Sciences

Aptose today also announced an exclusive drug discovery partnership with Laxai Avanti Life Sciences (LALS) for their expertise in next generation epigenetic-based therapies. Under the agreement, LALS will be responsible for developing multiple clinical candidates, including optimizing candidates derived from Aptose’s relationship with the Moffitt Cancer Center. Aptose will own global rights to all newly discovered candidates characterized and optimized under the collaboration, including all generated intellectual property.

"We have identified LALS as an organization with high-caliber medicinal chemistry and with robust, and highly efficient drug discovery capabilities that complement our capabilities at Aptose," said Dr. Rice. "These collaborations are designed to build upon insights into the epigenetic field that were informed by the mechanism of APTO-253. As we continue to advance APTO-253 into late-stage clinical development, we are committed to creating and acquiring additional differentiated agents and building a staged oncology pipeline behind APTO-253."

About APTO-253

Epigenetic suppression of the KLF4 gene has been reported in the scientific literature as a key transforming event in AML and high-risk myelodysplastic syndromes. APTO-253, Aptose’s lead drug candidate, is a first-in-class inducer of the Krüppel-like factor 4 (KLF4) tumor suppressor gene, and the only clinical-stage compound targeted for patients with suppressed KLF4 levels. APTO-253 has demonstrated a favorable safety profile with no evidence of bone marrow suppression. Preclinical studies have shown potent single-agent activity and an opportunity for combination therapy with a variety of anti-cancer therapeutics. The drug candidate is in a Phase 1b clinical study in patients with relapsed or refractory hematologic malignancies.

About Moffitt Cancer Center

Located in Tampa, Moffitt is one of only 45 National Cancer Institute-designated Comprehensive Cancer Centers, a distinction that recognizes Moffitt’s excellence in research, its contributions to clinical trials, prevention and cancer control. Moffitt is the top-ranked cancer hospital in Florida and has been listed in U.S. News & World Report as one of the "Best Hospitals" for cancer care since 1999. With more than 4,600 team members, Moffitt has an economic impact in the state of $1.9 billion. For more information, visit MOFFITT.org, and follow the Moffitt momentum on Facebook, Twitter and YouTube.

About Laxai Avanti Life Sciences

Laxai Avanti Life Sciences (LALS) was established in 2007 with a vision to innovate and accelerate the drug discovery campaigns of global pharmaceutical companies. The goal of LALS is to provide intelligent solutions to global pharmaceutical and biotechnological companies by providing high quality services with accelerated timelines. LALS provides a one-stop service for pharmaceutical and biotechnology companies around the globe to accelerate drug discovery programs. LALS current client base includes Biopharmaceutical, Agrochemical and Specialty Chemical Companies in Europe and the US.

On November 10, 2015 Loxo Oncology, Inc. (Nasdaq:LOXO), a biopharmaceutical company innovating the development of highly selective medicines for patients with genetically defined cancers, reported financial results for the third quarter ended September 30, 2015 and provided an update on its pipeline (Press release, Loxo Oncology, NOV 10, 2015, View Source [SID:1234508164]). Loxo Oncology will not be conducting a conference call in conjunction with this earnings release.

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"In the third quarter we made tremendous progress with LOXO-101, executing ahead of plan," said Josh Bilenker, M.D., chief executive officer of Loxo Oncology. "Our Phase 1 trial continues to mature nicely, and we were able to open our Phase 2 trial approximately six months early. Additionally, we were proud to report that the National Cancer Institute selected LOXO-101 as the preferred and sole TRK inhibitor for relevant patients in the NCI-MATCH trial. I think we can attribute much of this success to the compelling efficacy and tolerability signals seen in Phase 1, and a growing appreciation for the diversity of TRK fusion biology across human cancer in the scientific and molecular diagnostic communities."

Program Updates

Loxo Oncology provided the following updates on its development programs:

LOXO-101: the only potent, oral, selective inhibitor of the tropomyosin receptor kinase (TRK) family of proteins in clinical development

LOXO-101 Phase 2 Trial Initiated

Loxo Oncology enrolled the first patient in its Phase 2 trial of LOXO-101, a global, multi-center, single-arm, open-label basket trial in approximately up to 150 adult patients with solid tumors that harbor a TRK fusion, as determined by any Clinical Laboratory Improvement Amendments (CLIA) certified or equivalently-accredited test. Patients with TRK fusions will be enrolled into one of eight cohorts: non-small cell lung cancer, thyroid cancer, sarcoma, colorectal cancer, salivary gland cancer, biliary cancer, primary central nervous system tumors and all other solid tumor histologies.

LOXO-101 Phase 1 Data Presented at EORTC

New results from the ongoing dose-escalation Phase 1 study of LOXO-101 in patients with solid tumors refractory to standard therapy were reported in a late-breaking oral presentation at the 27th AACR (Free AACR Whitepaper)-NCI-EORTC Symposium on Molecular Targets and Cancer Therapeutics.

As of the October 20, 2015 data cutoff date, 30 patients had been enrolled and treated, including six patients with cancers harboring TRK fusions. Three of the six patients with TRK fusion cancers had been on study sufficiently long for their first efficacy assessment, and all three had achieved an objective response at the first response assessment, as defined by standard RECIST criteria. All three of these patients remain in response and on study. The other three patients with TRK fusion cancers were recently enrolled and thus had not yet been evaluated for response as of the data cutoff date, though they all remain on study.
LOXO-101 has been well tolerated, including the 100 mg twice-daily dose, which has been selected for Phase 2 study and has shown efficacy in TRK fusion patients. The majority of adverse events reported by investigators have been mild to moderate. A maximum tolerated dose (MTD) has not been defined, though near-term Phase 1 enrollment will focus on further characterizing the pharmacokinetics and safety of the 100 mg twice-daily dose dosing. The data presentation from the meeting can be accessed here View Source

LOXO-101 Selected for NCI-MATCH Trial

The independent committee of the National Cancer Institute-Molecular Analysis for Therapy Choice (NCI-MATCH) clinical trial chose LOXO-101 as the sole, dedicated treatment arm for patients with TRK gene fusions.

The NCI-MATCH trial will initially enroll 3,000 patients with tumor biopsies available for comprehensive genomic profiling and assign these patients to an appropriate targeted therapy arm based on the molecular abnormalities of each tumor. Over 700 trial sites in 48 states in the United States are currently open for enrollment.

LOXO-101 Granted Orphan Drug Designation

The United States Food and Drug Administration (FDA) granted Loxo Oncology orphan drug designation for LOXO-101 for treatment of patients with soft tissue sarcoma.

Pre-clinical Programs

Data on RET and FGFR Programs Presented at AACR (Free AACR Whitepaper)-NCI-EORTC

Loxo presented two preclinical posters at AACR (Free AACR Whitepaper)-NCI-EORTC containing the first publicly disclosed data for its Rearranged during Transfection (RET) and Fibroblast Growth Factor Receptor (FGFR) programs.

Loxo Oncology’s novel, potent and selective RET inhibitor demonstrated potent inhibition of RET in enzyme and cellular assays with minimal activity against highly related kinases in animal models. The company is on track to initiate a Phase 1 study of its RET inhibitor in late 2016 or early 2017.

Data for the company’s potent and selective FGFR inhibitor show that it spared FGFR1 and other related kinases and possesses high oral bioavailability and favorable PK properties in animal models.

Third Quarter 2015 Financial Results

As of September 30, 2015 Loxo had aggregate cash, cash equivalents and investments of $93.4 million, compared to $112.9 million as of December 31, 2014.

The company continues to expect cash burn of $30-$33 million in 2015, and based on the current operating plan, the company believes existing capital resources will be sufficient to fund anticipated operations into 2017.

Research and development expenses were $6.3 million for the third quarter 2015 compared to $5.1 million for the third quarter 2014. The increase was primarily due to expanded Phase 1 and Phase 2 clinical development activities for LOXO-101 and additional full-time equivalents and other support dedicated to discovery, preclinical, and manufacturing activities at Array BioPharma. The company also recognized R&D-related stock-based compensation expense of $0.5 million during the third quarter of 2015 compared to $1.7 million for the third quarter of 2014.

Research and development expenses were $15.8 million for the nine months ended September 30, 2015 compared to $9.9 million for the nine months ended September 30, 2014. The increase was primarily due to expanded Phase 1 and Phase 2 clinical development activities for LOXO-101 and additional full-time equivalents and other support dedicated to discovery, preclinical, and manufacturing activities at Array BioPharma. The company also recognized R&D-related stock-based compensation expense of $1.8 million during the nine months ended September 30, 2015 compared to $2.0 million for the nine months ended September 30, 2014.

General and administrative expenses were $2.6 million for the third quarter 2015 compared to $1.6 million for the third quarter 2014. The increase was primarily due to additional full-time equivalents, increased compensation costs and increased costs associated with operating as a public company. The company also recognized G&A-related stock-based compensation expense of $0.7 million during the third quarter of 2015 compared to $0.3 million for the third quarter of 2014.

General and administrative expenses were $7.3 million for the nine months ended September 30, 2015 compared to $3.6 million for the nine months ended September 30, 2014. The increase was primarily due to additional full-time equivalents, increased compensation costs and increased costs associated with operating as a public company. The company also recognized G&A-related stock-based compensation expense of $2.0 million during the nine months ended September 30, 2015 compared to $0.5 million for the nine months ended September 30, 2014.

Net loss attributable to common stockholders was $8.8 million and $23.0 million for the three and nine months ended September 30, 2015, respectively, compared to $6.7 million and $13.6 million for the three and nine months ended September 30, 2014, respectively.

About LOXO-101

LOXO-101 is a potent, oral and selective investigational new drug in clinical development for the treatment of patients with cancers that harbor abnormalities involving the tropomyosin receptor kinases (TRKs). Growing research suggests that the NTRK genes, which encode for TRKs, can become abnormally fused to other genes, resulting in growth signals that can lead to cancer in many sites of the body. In an ongoing Phase 1 clinical trial, LOXO-101 has demonstrated encouraging preliminary efficacy. LOXO-101 is also being evaluated in a global Phase 2 multi-center basket trial in patients with solid tumors that harbor TRK gene fusions. For additional information about both the LOXO-101 clinical trials, please refer to www.clinicaltrials.gov. Interested patients and physicians can contact the Loxo Oncology Physician and Patient Clinical Trial Hotline at 1-855-NTRK-123.

On November 10, 2015 FUJIFILM Corporation (President: Shigehiro Nakajima) reported to conduct a clinical trial of its anti-cancer drug FF-10101 in patients with relapsed or refractory acute myeloid leukemia (AML) in the United States next year (Press release, Fujifilm, NOV 10, 2015, View Source [SID:1234508186]). FF-10101 is a new drug candidate discovered by Fujifilm, tapping into its advanced technology to synthesize and design chemical compounds nurtured through the photographic film business.

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AML is a type of hematological malignancy and considered as a refractory disease. The malignant transformation of hematopoietic stem cells into leukemia cells followed by their abnormal growth in bone marrow inhibits normal hematopoietic functions, leading to cytopenia. Organ dysfunctions are also caused by infiltration of the leukemia cells out of the bone marrow. Fms-like tyrosine kinase 3 (FLT3)* is a protein involved in proliferation of hematopoietic cells. Approximately 30% of AML patients harbor FLT3 mutations such as internal tandem duplications (ITD)** and tyrosine kinase domain (TKD)*** mutations, which induce abnormal growth of leukemia cells. Currently, FLT3 inhibitors resulting to inhibit leukemia cell proliferation are being developed, some of which show a favorable efficacy against leukemia cells with FLT3-ITD mutation. However, the TKD mutations are generally known to cause drastic decrease of efficacies of the FLT3 inhibitors.

FF-10101 is a FLT3 inhibitor which binds to an amino acid in FLT3 irreversibly. FF-10101 demonstrated a high efficacy in reducing leukemia cells with the ITD or TKD mutation in a preclinical mouse model, hence the promising efficacy in clinical trials is expected. The results of the preclinical study will be presented at the 57th annual meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper), the world’s largest hematology meeting, in Orlando, Florida the United States in December this year.

The development of FF-10101 was adopted as Next generation Technology Program (NexTEP) by the Japan Science and Technology Agency, which is in collaboration with Professor Hitoshi Kiyoi, M.D., Ph.D., Nagoya University, to investigate the efficacy and the safety profile of FF-10101. Findings from the research will be applied to the clinical study in an effort to further accelerate the development of FF-10101.

Fujifilm is defining oncology as its focal area and promoting the R&D of anti-cancer drugs by combining the technologies and experiences including chemical synthesis capacity, design ability, analysis technology accumulated through the development and production of photographic film. Fujifilm has initiated a Phase I clinical trial of FF-10501 in patients with relapsed or refractory myelodysplastic syndromes (MDS)*4. The company will keep focusing on unmet medical needs in fields including oncology and actively promote R&D to expand business deployment and supply of innovative pharmaceutical products so as to contribute to resolving social issues.