Intensity Therapeutics Presents Positive Preliminary Phase 1/2 Results for Intratumoral Injection of INT230-6 at ASCO 2019

On June 1, 2019 Intensity Therapeutics, Inc., a clinical-stage biotechnology company pioneering a novel, immune-based approach to treat solid tumor cancers through direct injection of its proprietary therapeutic agents, reported positive preliminary results from the company’s ongoing Phase 1/2 clinical trial of its lead product candidate, INT230-6, in a poster at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting in Chicago (Press release, Intensity Therapeutics, JUN 1, 2019, View Source [SID1234536755]).
The poster highlights the results of 34 patients with 15 different types of advanced or metastatic solid tumors that have failed all or are not candidates for approved, available therapies.

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INT230-6 was well tolerated in doses up to 120 mL, including intratumoral dosing into more than 100 tumors deep in the body. The 120 mL dose of INT230-6 contains amounts of the cytotoxic agents greater than a typical intravenous (IV) dose. Based on comparisons to historical IV data of the active agents comprising INT230-6, the observed pharmacokinetic profiles indicate that drug remains mostly in the tumor following INT230-6 dosing. While the trial is aimed at assessing safety, several patients have shown tumor shrinkage and prolonged disease control after completing INT230-6 treatment. The results show greater benefit in patients who have received higher doses, and who have had multiple tumors injected. Dose escalation is ongoing.

Additionally, the immune activation data observed was consistent with nonclinical data, as local delivery of INT230-6 into tumors induced an immune response with increases of CD4+ and CD8+ T-cells in the blood and in the tumor microenvironment without any immune-related adverse events. Several patients have had shrinkage of non-injected tumors indicating an abscopal response.

"We are excited and encouraged by the positive preliminary results of our Phase 1/2 trial," said Lewis H. Bender, President and Chief Executive Officer of Intensity Therapeutics. "It is our aim to improve cancer treatment, reduce the side effects associated with systemic therapies and improve patient outcomes using intratumorally dosed INT230-6."

"The patients in our trial have a tremendous need for a new therapy. They have failed a median of three prior treatments with a number of patients having progressed following seven or more drug therapies," said Ian B. Walters, MD, Chief Medical Officer of Intensity Therapeutics. "Thus far, the data indicate that direct intratumoral injection of our product minimizes systemic side effects while promoting an augmented natural immune response that can fight a patient’s cancer for several months following completion of our treatment."

Details of the poster presentation are as follows:

Title: Safety profile of INT230-6, a novel intratumoral (IT) formulation, during injections into a variety of refractory deep and superficial tumors with evidence of tumor regression and immune activation

Abstract Number: 2602

Date/Time: Saturday, June 1, 2019, 8-11 a.m. CDT

Poster Session: Developmental Immunotherapy and Tumor Immunobiology

Presenter: Anthony El-Khoueiry, MD, Associate Professor of Clinical Medicine and Director of the Phase I Drug Development Clinical Program, University of Southern California

About INT230-6

INT230-6, Intensity’s lead proprietary product candidate, is designed for direct intratumoral injection. The drug is comprised of two proven, potent anti-cancer agents and a penetration enhancer molecule that helps disperse the drugs throughout tumors and diffuse into cancer cells. INT230-6 is being evaluated in a Phase 1/2 clinical study (NCT03058289) in patients with various advanced solid tumors. In preclinical studies, INT230-6 eradicated tumors by a combination of direct tumor kill and recruitment of dendritic cells to the tumor micro-environment that induced anti-cancer T-cell activation. Treatment with INT230-6 in in vivo models of severe cancer resulted in substantial improvement in overall survival compared to standard therapies. Further, INT230-6 provided complete responder animals with long-term, durable protection from multiple re-inoculations of the initial cancer and resistance to other cancers. In mouse models, INT230-6 has shown strong synergy with checkpoint blockage, including anti-PD-1 and anti-CTLA4 antibodies. INT230-6 was discovered from Intensity’s DfuseRxSM platform.

Celldex Announces Data from CDX-3379 Clinical Program Presented at ASCO 2019; Promising Biomarker Strategy Identified for Head and Neck Squamous Cell Carcinoma

On June 1, 2019 Celldex Therapeutics, Inc. (NASDAQ:CLDX) reported results from the CDX-3379 clinical program at the 2019 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting in Chicago (Press release, Celldex Therapeutics, JUN 1, 2019, View Source [SID1234536771]). To date, three studies of CDX-3379 have enrolled patients with head and neck squamous cell carcinoma (HNSCC), including the ongoing Phase 2 exploratory study of CDX-3379 in combination with Erbitux (cetuximab) in patients with cetuximab-resistant, advanced human papillomavirus (HPV) negative HNSCC who have previously been treated with an anti-PD1 checkpoint inhibitor.

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Emerging data from the Phase 2 study and earlier studies of CDX-3379 suggest that antitumor activity may be associated with somatic mutations in certain genes. Based on these observations, Celldex conducted an exploratory biomarker analysis in 18 HNSCC patients across the CDX-3379 clinical development program. These results support the further development of CDX-3379 in biomarker-selected patient populations and were highlighted during a presentation at ASCO (Free ASCO Whitepaper) by Julie E. Bauman, MD, MPH, Professor of Medicine, Chief, Division of Hematology and Oncology, Associate Director, Translational Research, University of Arizona Cancer Center, lead author for the poster and an investigator in the Phase 2 study.

"We have observed intriguing clinical activity across a number of patients with similar gene mutation patterns in a disease that has extremely limited treatment options and a particularly poor prognosis," said Dr. Bauman. "While the data are early, they are provocative and suggest the potential for a biomarker enrichment strategy that could change the standard of care for these patients. I look forward to the opportunity to obtain additional data on CDX-3379 in biomarker selected patient populations."

CDX-3379 is a human monoclonal antibody that uniquely blocks the activity of ErbB3 (HER3). ErbB3 is expressed in many cancers, including head and neck squamous cell cancer (HNSCC) and is believed to be an important receptor regulating cancer cell growth and survival as well as resistance to targeted therapies.

Biomarker analysis

Next-generation sequencing was performed on tumor samples from 18 patients with HNSCC treated with CDX-3379 across the three clinical studies. This data set included four patients with clinical responses, including two durable complete responses (11+ months and 8.3 months), an exceptional partial response (greater than 92% tumor shrinkage) and an unconfirmed partial response; eight patients with stable disease and/or tumor shrinkage; and, six patients with progressive disease.

Across the CDX-3379 program, FAT1 and NOTCH1, NOTCH2, or NOTCH3 mutations and primary tumor site of oral cavity were associated with clinical activity (clinical response, tumor shrinkage and stable disease) in HNSCC
All four clinical responses occurred in patients with FAT1 mutations
All four clinical responses occurred in patients with a primary tumor site of oral cavity
Three of the four clinical responses occurred in patients who also had NOTCH1, NOTCH2 or NOTCH3 mutations
Also, of note, all patients (n=7 of 18) who experienced clinical benefit (objective response or stable disease greater than or equal to 12 weeks) had FAT1 and/or NOTCH1-3 mutations.
Current literature suggests that loss of FAT1 function results in activation of the transcriptional cofactor YAP11; YAP1 has been shown to upregulate components of ErbB signaling pathways2,3, including the ErbB3 ligand NRG14
Inactivating mutations in the FAT1 and NOTCH genes have been identified in 32% and 26% of HPV(-) HNSCC tumors, respectively5
Preclinical studies investigating the association of CDX-3379 sensitivity and inactivating mutations of FAT1 and other genes are ongoing

Phase 2 CDX-3379 Study Results and Next Steps

This multicenter, open-label, Phase 2 study of CDX-3379 in combination with cetuximab is designed to enroll approximately 30 patients with cetuximab-resistant, advanced, HPV negative HNSCC who have previously been treated with an anti-PD1 checkpoint inhibitor, a population with limited options and a particularly poor prognosis. Cetuximab is dosed weekly (initial dose at 400 mg/m2 IV, then 250 mg/m2 IV); CDX-3379 (12 mg/kg IV) is administered once every three weeks. Treatment continues until disease progression or intolerance, and assessments occur every six weeks. Using a Simon two-stage design, the first stage of study was designed to enroll 13 patients, and if at least one patient achieved a partial response or complete response, enrollment could progress to the second stage; this objective was met.

Fifteen patients were enrolled in stage 1 of the study. Patients had a median of 3 (range of 2-6) prior cancer therapy treatments. All patients had received prior checkpoint inhibitor treatment and 14 of 15 patients were cetuximab refractory. Notable clinical activity was observed in this refractory patient population where treatment options are limited.

A durable confirmed complete response (11+ months) was observed; this response remains ongoing and the patient continues to receive treatment.
An unconfirmed partial response (uPR) in a patient that had not received cetuximab was also observed.
7 patients experienced stable disease (47%; includes uPR).
A clinical benefit rate of 29% was achieved (objective response or stable disease greater than or equal to 12 weeks).
Dose reductions and/or delays to the combination therapy in the majority of patients may have impacted the magnitude of anti-tumor activity; dose modifications are being considered for future studies.
CDX-3379 in combination with cetuximab was generally associated with the expected target-mediated adverse events of diarrhea and rash.
Celldex intends to incorporate evaluation of biomarkers for patient selection into the CDX-3379 development program, either through amending the existing study or concluding the study and initiating a new clinical trial. The Company, working together with investigators and key opinion leaders in the treatment of HNSCC, anticipates finalizing these plans in the coming weeks.

Erbitux is a registered trademark of Eli Lilly & Co.
1Martin D, Nat Commun 2018. 2Zhang J, Nat Cell Biol 2009. 3Wang C, Cancer Res 2017. 4He C, Oncogene 2015. 5Cancer Genome Atlas Network, Nature 2015.

About CDX-3379
CDX-3379 is a human immunoglobulin G1 lambda (IgG1λ) monoclonal antibody that selectively binds and inhibits ErbB3 activity. ErbB3 may be an important receptor regulating cancer cell growth and survival as well as resistance to targeted therapies, and it is expressed in many cancers, including head and neck, thyroid, breast, lung and gastric cancers, as well as melanoma. The proposed mechanism of action for CDX-3379 sets it apart from other drugs in development in this class due to its ability to block both ligand-independent and ligand-dependent ErbB3 signaling by binding to a unique epitope. It has a favorable pharmacologic profile, including a longer half-life and slower clearance relative to other drug candidates in this class. CDX-3379 also has potential to enhance anti-tumor activity and/or overcome resistance in combination with other targeted and cytotoxic therapies to directly kill tumor cells.

Daiichi Sankyo’s Pexidartinib Demonstrated Further Improvement with Continued Treatment of Tenosynovial Giant Cell Tumor Patients in New Long-Term Analysis Presented at 2019 ASCO Annual Meeting

On June 1, 2019 Daiichi Sankyo Company, Limited (hereafter, Daiichi Sankyo), reported that new data from a pooled analysis of the phase 3 ENLIVEN study and phase 1 extension study showed continued treatment with pexidartinib resulted in an increased tumor response rate in TGCT patients (Press release, Daiichi Sankyo, JUN 1, 2019, https://www.prnewswire.com/news-releases/daiichi-sankyos-pexidartinib-demonstrated-further-improvement-with-continued-treatment-of-tenosynovial-giant-cell-tumor-patients-in-new-long-term-analysis-presented-at-2019-asco-annual-meeting-300860162.html [SID1234536787]). The data will be presented during a Poster Session on Saturday, June 1, at the 2019 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting in Chicago (Abstract #11042; 8:00-11:00 a.m. CDT).

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The long-term pooled results showed the best overall response with pexidartinib at a median treatment duration of 17 months was 54 percent by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 and 64 percent by Tumor Volume Score (TVS). The median duration of response was not reached.

The safety profile of pexidartinib in the long-term follow-up was consistent with what has been seen in previous analyses. Across the studies, the most frequent adverse events were hair color change (75%), fatigue (60%), nausea (45%), arthralgia (38%), aspartate aminotransferase (AST) increase (30%) and diarrhea (30%). Pexidartinib was associated with two clinically distinct types of hepatic adverse reactions. The first was frequent dose-dependent aminotransferase elevations that may be a pharmacologic effect of CSF1R inhibition. The second hepatic adverse reaction was an idiosyncratic serious mixed or cholestatic hepatotoxicity. Across the pexidartinib clinical program, there were two irreversible cases of cholestatic liver injury, both in non-TGCT study populations. One patient died with advanced cancer and ongoing liver toxicity and one patient required a liver transplant.1

"Looking across the longer-term findings from both the pivotal phase 3 trial and phase 1 extension study, the results demonstrated continued and improved effect of pexidartinib in reducing tumor size in TGCT patients," said A.J. Gelderblom, MD, Chair of the Department of Medical Oncology at the Leiden University Medical Center and an ENLIVEN investigator. "This is important because TGCT is often a chronic disease, and we do not have effective treatment options for patients whose TGCT is inoperable or for which surgery would likely be associated with severe morbidity or functional limitations, like those enrolled in the studies."

Additional data published online ahead of ASCO (Free ASCO Whitepaper) (Abstract #e22527) further highlight the need for new treatment options, showing that TGCT patients missed more time from work due to disability and medical visits. The disability burden seen was greater in patients receiving surgery.

"We are pleased to share additional data that reinforce the potential of pexidartinib to offer clinically meaningful improvement for select patients with TGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery," said Dale Shuster, Ph.D., Executive Director, Global Oncology R&D, Daiichi Sankyo. "We look forward to working with regulatory authorities and delivering on our goal to help address the significant unmet need that exists in the treatment of this rare and debilitating tumor."

About the Phase 1 Extension Study
Patients enrolled in this phase 1 single-arm, multi-center, extension cohort study included those with a histologically confirmed diagnosis of TGCT with demonstrated tumor progression within the past year that was recurrent, inoperable or resectable but requiring extensive surgery. Following baseline assessment, the efficacy of pexidartinib was assessed radiologically every two months utilizing RECIST 1.1 criteria and TVS. Patients remained on treatment until disease progression or drug intolerance.

Interim data from the phase 1 study were published in The New England Journal of Medicine.2

About the ENLIVEN Study
ENLIVEN, a double-blind, randomized, global multi-center, pivotal phase 3 study, evaluated pexidartinib in patients with symptomatic advanced TGCT for whom surgical removal of the tumor would be associated with potentially worsening functional limitation or severe morbidity. The first part of the study, the double-blind phase, enrolled 120 patients who were randomized (1:1) to receive either pexidartinib or placebo at 1000 mg/day for 2 weeks followed by 800 mg/day for 22 weeks in order to evaluate the efficacy and safety of pexidartinib versus placebo. The primary endpoint of the study was the percentage of patients achieving a complete or partial response after 24 weeks of treatment (Week 25), as assessed with centrally-read MRI scans using RECIST 1.1 criteria. Key secondary endpoints included range of motion, response by tumor volume score, PROMIS physical function, stiffness, and measures of pain reduction.

After completing the first part of the study, patients randomized to either pexidartinib or placebo were eligible to take part in the second part of ENLIVEN, a long-term, open-label part where patients could continue to receive or start to receive pexidartinib. In October 2016, following two reported cases of serious, non-fatal liver toxicity in the ENLIVEN study, the data monitoring committee (DMC) recommended that patients receiving placebo in the first part of the study should no longer be eligible to start pexidartinib in the second part of the study. A total of 120 patients who were enrolled prior to the DMC recommendation continued with the study according to the revised protocol.

About TGCT (PVNS/GCT-TS)
TGCT, also referred to as pigmented villonodular synovitis (PVNS) or giant cell tumor of the tendon sheath (GCT-TS), is a rare, nonmalignant tumor that can be locally aggressive. TGCT affects the synovium-lined joints, bursae and tendon sheaths, resulting in swelling, pain, stiffness and reduced mobility in the affected joint or limb.3, 4, 5

While the exact incidence of TGCT is not known, it is estimated that the incidence of TGCT is 11 to 50 cases per million person-years, based on studies from three countries.6, 7, 8 TGCT is subcategorized into two types: localized, which is more common and accounts for 90 percent of cases, and diffuse, which accounts for 10 percent of cases.7,8 The current standard of care for TGCT is surgical resection.3,4 However, in patients with a recurrent, difficult-to-treat or diffuse form where the tumor can wrap around bone, tendons, ligaments and other parts of the joint, it is more difficult to remove or might not be amenable to improvement with surgery due to the risk of morbidity and potential recurrence. Additional surgeries for more severe cases can lead to significant joint damage, debilitating functional impairments and reduced quality of life, and amputation may be considered.9, 10, 11

Recurrence rates for localized TGCT are estimated to be up to 15 percent following complete resection.4,12,13,14 Diffuse TGCT recurrence rates are estimated to be about 20 to 50 percent following complete resection.5,12,15 TGCT affects all age groups; the diffuse type, on average, occurs most often in people below the age of 40, and the localized type typically occurs in people between 30 and 50 years old. 3,6,7,8

About Pexidartinib
Pexidartinib is an investigational, novel, oral small molecule that potently inhibits the colony stimulating factor-1 receptor (CSF1R), which is a primary growth driver of abnormal cells in the synovium that cause TGCT. Pexidartinib also inhibits c-kit and FLT3-ITD. Pexidartinib was discovered by Plexxikon Inc., the small molecule structure-guided R&D center of Daiichi Sankyo.

Pexidartinib is currently under regulatory review with the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the treatment of for adult patients with symptomatic TGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery. In addition to Priority Review designation, pexidartinib has been granted Breakthrough Therapy designation for the treatment of patients with pigmented villonodular synovitis (PVNS) or giant cell tumor of the tendon sheath (GCT-TS), where surgical resection may result in potentially worsening functional limitation or severe morbidity, and Orphan Drug designation for PVNS/GCT-TS by the FDA. Pexidartinib also has received Orphan Drug designation from the European Commission for the treatment of TGCT.

Pexidartinib is an investigational compound that has not been approved for any indication in any country. Safety and efficacy have not been established.

About Daiichi Sankyo Cancer Enterprise
The mission of Daiichi Sankyo Cancer Enterprise is to leverage our world-class, innovative science and push beyond traditional thinking to create meaningful treatments for patients with cancer. We are dedicated to transforming science into value for patients, and this sense of obligation informs everything we do. Anchored by three pillars including our investigational Antibody Drug Conjugate Franchise, Acute Myeloid Leukemia Franchise and Breakthrough Science, we aim to deliver seven distinct new molecular entities over eight years during 2018 to 2025. Our powerful research engines include two laboratories for biologic/immuno-oncology and small molecules in Japan, and Plexxikon Inc., our small molecule structure-guided R&D center in Berkeley, CA. Compounds in pivotal stage development include: [fam-] trastuzumab deruxtecan, an antibody drug conjugate (ADC) for HER2 expressing breast, gastric and other cancers; quizartinib, an oral selective FLT3 inhibitor, for newly-diagnosed and relapsed/refractory FLT3-ITD acute myeloid leukemia (AML); and pexidartinib, an oral CSF1R inhibitor, for TGCT. For more information, please visit: www.DSCancerEnterprise.com.

MEI Pharma Presents Clinical Results for ME-344 in Combination with Bevacizumab in Early HER2 Negative Breast Cancer Patients at the 2019 American Society of Clinical Oncology (ASCO) Annual Meeting

On June 1, 2019 MEI Pharma, Inc. (NASDAQ: MEIP), a late-stage pharmaceutical company focused on advancing potential new therapies for cancer, reported data presented at ASCO (Free ASCO Whitepaper) 2019 from an investigator-initiated study of investigational ME-344 in combination with bevacizumab (marketed as Avastin) in patients with early HER2-negative breast cancer (Press release, MEI Pharma, JUN 1, 2019, View Source [SID1234536756]). This study demonstrated proof of biologic anti-tumor activity as measured by a statistically significant reduction in Ki67, a measure of cell proliferation that is highly correlated with tumor response, in the group of patients treated with ME-344 compared to an increase in the group receiving saline.

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"Data from this clinical study of ME-344 in combination with bevacizumab represents a potential novel approach to disrupting tumor metabolism and limiting tumor proliferation by inhibiting the heightened energy production necessary for cell division and cancer growth," stated the study principal investigator, Miguel Quintela-Fandino, M.D., Ph.D., Director of the Clinical Research Program, Centro Nacional De Investigaciones Oncologicas, Madrid, Spain. "These results offer evidence for the biologic antitumor activity of ME-344 in certain metabolic contexts and support further exploration of the mitochondrial inhibitor ME-344 in a therapeutic role, providing a potential novel mechanism that may improve patient outcomes in combination with antiangiogenic therapeutics such as bevacizumab."

The ME-344 ASCO (Free ASCO Whitepaper) 2018 poster can be accessed on the MEI Pharma website.

ME-344 Clinical Data
The clinical study was a multicenter, investigator-initiated, randomized, open-label trial evaluating ME-344 in a total of 42 patients with early HER2-negative breast cancer in combination with the vascular endothelial growth factor inhibitor bevacizumab. Patients were randomized one-to-one to either ME-344 plus bevacizumab or saline plus bevacizumab.

The primary objective of the study was to show proof of ME-344 biologic activity as measured by Ki67 reductions from day 0 to 28 compared to placebo. Secondary objectives included determining whether ME-344 biologic activity correlates with vascular normalization. The data demonstrate significant biologic activity in the ME-344 treatment group:

In ME-344 treated patients, mean absolute Ki67 decreases were 13.3 compared to an increase of 1.1 in the bevacizumab monotherapy group (P=0.01).
In ME-344 treated patients, mean relative Ki67 decreases were 23% compared to an increase of 186% in the bevacizumab monotherapy group (P < 0.01).
The mean relative Ki67 reduction in patients experiencing vascular normalization in the ME-344 treated patients was 33%, compared to an increase of 11.8% in normalized patients from the bevacizumab monotherapy group (P=0.09). Approximately one-third of patients in each arm had vascular normalization.
Treatment was generally well tolerated; two Grade 3 adverse events of high blood pressure were reported, 1 in each arm, and deemed related to bevacizumab.

About ME-344
ME-344 is a novel, tumor selective, isoflavone-derived mitochondrial inhibitor drug candidate. It directly targets the OXPHOS complex 1, a pathway involved in the production of adenosine triphosphate, or ATP, in the mitochondria. Treatment of tumor cells with ME-344 results in a rapid loss of ATP and cancer cell death. ME-344 demonstrated evidence of single-agent activity against refractory solid tumors in a Phase I study, and in preclinical studies, tumor cells treated with ME-344 resulted in a rapid loss of ATP and cancer cell death.

In addition to single-agent activity, ME-344 may also have potential in combination with antiangiogenic therapeutics. While antiangiogenics reduce the rate of glycolysis in tumors as a mechanism to block growth, tumor metabolism often shifts to mitochondrial metabolism to continue energy production to support continued tumor proliferation. In such cases of tumor plasticity in the presence of treatment with antiangiogenics, targeting the alternative metabolic source with ME-344 may open an important therapeutic opportunity.

Positive results of lurbinectedin Phase II trial (PharmaMar) for the treatment of relapsed small cell lung cancer are presented at ASCO

On June 1, 2019 The results of PharmaMar’s (MSE: PHM) Phase II study with lurbinectedin as a single agent for the treatment of relapsed small cell lung cancer were presented to the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) conference, which is currently being held in Chicago. The results of this trial, which achieved its primary endpoint, have been presented orally by Dr. Luis Paz-Ares, Head of the Oncology Department at the Hospital Universitario 12 de Octubre in Madrid and lead author of the study.

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In his presentation entitled "Efficacy and safety profile of lurbinectedin in second-line SCLC patients: Results from a phase II single-agent trial", Dr.Paz-Ares updated the data from the lurbinectedin study, where an ORR of 35.2% in the total population, 45% in patients with sensitive disease (CTFI≥90 days, i.e., those who have suffered a relapse of the disease in a period greater than or equal to 90 days) and 22.2% in patients with resistant disease (CTFI<90 days, i.e., those patients who have suffered a relapse of the disease in a period less than 90 days) has been seen.

"Lurbinectedin is showing to be a new potential treatment alternative for second-line small cell lung cancer, where, until now, no progress has been made for more than two decades," says Dr. Luis Paz-Ares.

Additional Study Results

The Disease Control Rate (DCR) was 68.6% in the overall population, 81.7% in sensitive patients and 51.1% in resistant patients.
The median Duration of Response (DOR) was 5.3 months in the overall population, 6.2 months in sensitive patients and 4.7 months in resistant patients.
The median Progression Free Survival (PFS) was 3.9 months in the overall population, 4.6 months in sensitive patients, and 2.6 months in resistant patients.
The median OS was 9.3 months in the overall population, 11.9 months in sensitive patients, and 5.0 months in resistant patients.
"Having been chosen to present positive results at ASCO (Free ASCO Whitepaper) is an honor for any pharmaceutical company. These results demonstrate that lurbinectedin is a strong candidate to become a therapeutic alternative for patients with small cell lung cancer, a large unmet medical need," explains José María Fernández, President of PharmaMar.

In terms of product safety, lurbinectedin has shown a favorable and manageable safety profile. The most common treatment-related adverse effects have been neutropenia, nausea or vomiting, and fatigue.

Grade 3-4 neutropenia occurred in 22.9% of cases, grade 3-4 febrile neutropenia in only 4.8%, grade 3-4 anemia in 6.7%, and grade 3-4 thrombocytopenia in 4.8%.

By way of reference, the data provided for lurbinectedin compares favorably (non head-to-head) to the data included in the topotecan FDA label1, the last molecule approved for second-line treatment, in 1996. The topotecan arm saw an ORR of 24%, [median] PFS of 3.9 months and median OS of 5.8 months was seen. In terms of safety, topotecan showed grade 4 neutropenia in 70% of the patients, grade 3-4 febrile neutropenia in 28% and grade 3-4 anemia in 42%. The difference between the results of both these molecules, although not having comparable face-to-face studies, speaks of the potential of lurbinectedin as a potential new alternative treatment for second-line small cell lung cancer.

The single-agent lurbinectedin study is a single-arm, Phase II, multicenter trial, involving 105 patients recruited from 39 centers in 9 countries in Western Europe along with the USA, studying the safety and efficacy of lurbinectedin in second line treatment of small cell lung cancer.

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