A phase Ib study of NUC-3373 in combination with standard therapies in advanced/metastatic colorectal cancer (NuTide:302).

2021 ◽  
Vol 39 (3_suppl) ◽  
pp. 93-93
Author(s):  
Andrew L. Coveler ◽  
Farasat Kazmi ◽  
Kristen Keon Ciombor ◽  
Janet Graham ◽  
Lisa Jane Rodgers ◽  
...  
Keyword(s):  
Safety Profile ◽  
Safety Data ◽  
Resistance Mechanisms ◽  
Clinical Activity ◽  
Data Series ◽  
Rapid Progression ◽  
Phase Ib ◽  
Toxic Metabolites ◽  
Anti Cancer ◽  
Cancer Agent

93 Background: 5-FU is a key anti-cancer agent used across a broad range of tumors. The anti-cancer metabolite of 5-FU, fluorodeoxyuridine-monophosphate (FUDR-MP), binds and inhibits thymidylate synthase (TS), disrupting DNA synthesis and repair. 5-FU is often dosed with leucovorin (LV) to enhance the binding of FUDR-MP to TS. NUC-3373 is a targeted inhibitor of TS designed to bypass 5-FU resistance mechanisms associated with transport, activation and breakdown and avoid the generation of toxic metabolites such as FUTP and FBAL. NUC-3373 has a longer plasma t1/2 (~10 hours) than 5-FU (8-14 minutes), generating substantially higher intracellular levels of FUDR-MP and lower levels of the toxic metabolites FUTP and FBAL. Part 1 interim data from the NuTide:302 study demonstrated NUC-3373’s favorable PK and safety profile was unaffected by LV. Therefore, all subsequent patients in NuTide:302 are receiving NUC-3373 + LV. Here we present the next data series from NuTide:302. Methods: NuTide:302 is a 3-part, Phase Ib study in patients with advanced CRC who have relapsed after ≥2 prior lines of fluoropyrimidine- containing therapies. In Part 1, patients are receiving NUC-3373 with or without LV. In Part 2, NUC-3373 +LV is being administered in dose-escalation cohorts with either oxaliplatin (NUFOX) or irinotecan (NUFIRI). In Part 3, the NUFOX and NUFIRI regimens selected from Part 2 will be combined with biologics targeting VEGF and EGFR pathways. Results:36 patients have been treated in Part 1: 21 received 1500 mg/m2 NUC-3373 ± LV q2w; 11 received 1500 mg/m2NUC-3373 + LV q1w; and 4 received 2500 mg/m2 NUC-3373 + LV q1w. Clinical activity has been observed including tumor shrinkages and stabilization of disease for up to 5 months following rapid progression (≤2 months) on prior lines of therapy. One fluoropyrimidine-refractory patient demonstrated a 28% reduction in target lesions and achieved a stable disease of 5 months after rapid progression on CAPOX (2 months) and FOLFIRI (1.5 months). Safety data for all patients treated with NUC-3373 ± LV in Part 1 of NuTide:302 is shown below. Updated data on the clinical activity and safety of NUC-3373 will be presented. Clinical trial information: NCT03428958. Conclusions:NUC-3373 ± LV has shown clinical activity in heavily pre-treated CRC patients, including tumor shrinkage in a fluoropyrimidine-refractory patient. The safety profile of NUC-3373 ± LV is very encouraging: no neutropenia or hand-foot syndrome of any grade and no diarrhea or mucositis above Grade 2. NUC-3373 +LV is currently being dose escalated further in Part 1 and dosed with either oxaliplatin (NUFOX) or irinotecan (NUFIRI) in Part 2 of NuTide:302. [Table: see text]

NuTide:302: A phase Ib study to assess the safety, pharmacokinetics and clinical activity of the ProTide NUC-3373 when combined with standard agents used in colorectal cancer.

2019 ◽  
Vol 37 (4_suppl) ◽  
pp. TPS719-TPS719 ◽  
Author(s):  
T.R. Jeffry Evans ◽  
Sarah Patricia Blagden ◽  
Janet Shirley Graham ◽  
Kristen Keon Ciombor ◽  
Aimery De Gramont ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Human Study ◽  
Resistance Mechanisms ◽  
Primary Objective ◽  
Clinical Activity ◽  
Cancer Resistance ◽  
Phase Ib ◽  
Anti Cancer ◽  
Tumour Activity ◽  
Clinical Trial Information

TPS719 Background: Although 5-fluorouracil-based chemotherapies (5-FU, capecitabine, and floxuridine) remain the cornerstone of combination therapies for colorectal cancer (CRC), their clinical utility is limited by key cancer resistance mechanisms associated with breakdown, transport, and activation. These agents require intracellular conversion to the active metabolite fluorodeoxyuridine-monophosphate (FUDR-MP) before they can exert their core anti-cancer activity through inhibition of the enzyme thymidylate synthase (TS). NUC-3373 is a phosphoramidate transformation of FUDR-MP designed to bypass the key resistance mechanisms associated with 5-FU. Results from the first-in-human study of NUC-3373 (NuTide:301) in patients with advanced solid tumours demonstrated a favourable PK/PD profile for NUC-3373, with a longer plasma t1/2 (9.7 hours) than 5-FU (8-14 minutes) and much higher levels of the active anti-cancer metabolite, FUDR-MP (Ghazaly et alESMO, 2017). TS is efficiently inhibited and sequestered into TS-ternary complexes (TS-T), depleting the pool of dTMP within 2-4 hours. Methods: NuTide:302 is a two-part, Phase Ib study in patients with CRC who have relapsed after ≥ 2 prior lines of 5-FU-containing therapies. The primary objective is to identify a recommended NUC-3373 dose when administered every 2 weeks in combination with standard agents used in CRC treatment. Secondary objectives include safety, PK/PD, and anti‐tumour activity. In Part 1, approximately 12 patients will be administered NUC-3373 with leucovorin (LV) to determine if LV is beneficial in augmenting the formation of TS-T. If so, it will be administered in Part 2. In Part 2, the following combination agents will be administered with NUC-3373 (±LV): oxaliplatin; oxaliplatin + bevacizumab; oxaliplatin + panitumumab; irinotecan; and irinotecan + cetuximab. Up to 62 patients will be enrolled in cohorts of 3-6, in a modified 3+3 design. Enrollment to Part 1 initiated in September 2018. Clinical trial information: NCT03428958.

A phase I dose-escalation study of volasertib (BI 6727) combined with nintedanib (BIBF 1120) in advanced solid tumors.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 2556-2556 ◽  
Author(s):  
Filippo G. De Braud ◽  
Stefano Cascinu ◽  
Gianluca Spitaleri ◽  
Korinna Pilz ◽  
Laura Clementi ◽  
...  
Keyword(s):  
Solid Tumors ◽  
Safety Profile ◽  
Kinase Inhibitor ◽  
Standard Dose ◽  
Day Treatment ◽  
Single Agent ◽  
Safety Data ◽  
Clinical Activity ◽  
Advanced Solid Tumors ◽  
Dose Escalation Study

2556 Background: Volasertib (V) is a potent and selective cell cycle kinase inhibitor that induces mitotic arrest and apoptosis by targeting Polo-like kinases. Nintedanib (N) is a triple angiokinase inhibitor of VEGF, PDGF, and FGF receptors. Both have shown clinical activity with a manageable safety profile in patients (pts) with advanced solid tumors. This study was designed to determine the maximum tolerated dose (MTD) of V combined with N in these pts. Methods: Cohorts of 3–6 pts received V (100–450 mg IV Q3W) + oral standard dose N (200 mg BID continuously, except V infusion day). Treatment continued until clinical progression. Up to 12 pts were treated at the MTD for additional safety data. Primary endpoint was the MTD; secondary endpoints were pharmacokinetics (PK), overall safety, and preliminary efficacy. Results: 30 pts were treated (median age, 56.5 yr; ECOG PS 0/1/2, 33%/60%/7%; ≥3 prior therapies, 87%). At V doses >200 mg, 7 pts experienced 13 dose-limiting toxicities (DLTs) during cycle 1: increased alanine aminotransferase [ALT] or aspartate aminotransferase [AST], neutropenia and thrombocytopenia. The MTD was V 300 mg (Table). At the MTD, the most common all grade (Gr) adverse events (AEs) were neutropenia (69%), asthenia and thrombocytopenia (62% each), increased ALT, increased AST and diarrhea (54% each). Median (range) duration on treatment was 4 (1–18) cycles. Treatment was discontinued due to progressive disease (80%), DLT (3%) and other non-AE related reasons (17%). 2 objective responses were observed (1 complete [breast cancer] and 1 partial [NSCLC]), both with the 300 mg dose. 6 pts had SD for ≥ 6 mo. PK data will be presented at the meeting. Conclusions: MTD of V + standard dose N (200 mg BID) was determined to be 300 mg Q3W (the same as the recommended phase II single agent dose of V in solid tumors). This combination had a manageable safety profile without unexpected or overlapping toxicities and showed preliminary antitumor activity. Clinical trial information: NCT01022853. [Table: see text]

Anticancer activity in patients with advanced ovarian and biliary tract cancers treated with NUC-1031 and a platinum agent.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 3030-3030
Author(s):  
Sarah Patricia Blagden ◽  
Jennifer Bré ◽  
Peter Mullen ◽  
Chathunissa Gnanaranjan ◽  
Essam Ahmed Ghazaly ◽  
...  
Keyword(s):  
Biliary Tract ◽  
Single Agent ◽  
Nucleotide Metabolism ◽  
Clinical Activity ◽  
Phase Ib ◽  
Platinum Resistant ◽  
Anti Cancer ◽  
Platinum Agent ◽  
Cancer Activity

3030 Background: The inhibition of cellular nucleotide metabolism to promote apoptosis is a key principle of cancer therapy. This, in combination with platinum-induced DNA-damage, is key to promoting anti-cancer activity in a variety of tumors, including ovarian, biliary tract, lung, breast and bladder. NUC-1031, a phosphoramidate transformation of gemcitabine is designed to overcome resistance mechanisms that limit the efficacy of this nucleoside analog. NUC-1031 has shown broad clinical activity across multiple solid tumors as both a single agent and in combination with platinum agents. We show potential synergism between NUC-1031 and a platinum agent in advanced ovarian (OC) and biliary tract (BTC) cancers. Methods: PRO-002 was a phase Ib study; 25 patients (pts) with recurrent OC who had exhausted all other therapy options received NUC-1031 + carboplatin. 17 pts were considered platinum resistant (10) or platinum refractory (7). ABC-08 is a phase Ib study, 14 pts with advanced BTC treated in the first-line setting with NUC-1031 + cisplatin. Results: In PRO-002, strong efficacy signals were observed in non-platinum-responsive patients. Of the 17 response-evaluable platinum-resistant or refractory pts, 5 partial responses (PRs) and 11 stable diseases (SDs) were achieved, resulting in an ORR of 29% and a DCR of 94%. NUC-1031 + carboplatin was well-tolerated with no unexpected AEs; DLTs were myelosuppression and fatigue. Encouraging response rates were also observed in ABC-08 compared to historical standard of care (ABC-02). One CR (7%), 6 PRs (43%) and 1 SD (7%) were observed, resulting in an ORR of 50%. NUC-1031 + cisplatin was well-tolerated, with no unexpected AEs or DLTs. Complementary in vitro evidence suggests that the beneficial interaction occurs whereby platinum treatment sensitizes cells to NUC-1031. Conclusions: Increasing evidence suggests that NUC-1031 in combination with a platinum agent may have synergistic properties, leading to enhanced anti-cancer activity. In both OC and BTC, durable tumor shrinkage was observed. This was particularly encouraging in a platinum resistant/refractory OC population. Future studies utilizing both NUC-1031 plus a platinum agent will further elucidate the potential of this therapeutic combination.

Safety and tolerability of lapatinib in combination with taxanes (T) in patients with breast cancer (BC)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 1027-1027 ◽  
Author(s):  
J. P. Crown ◽  
H. A. Burris ◽  
S. Jones ◽  
K. M. Koch ◽  
A. Fittipaldo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Adverse Events ◽  
Safety Profile ◽  
Clinical Studies ◽  
Kinase Inhibitor ◽  
Safety Data ◽  
Systemic Exposure ◽  
Clinical Activity ◽  
Grade 3

1027 Background: Lapatinib (L) is an oral, dual ErbB1/B2 tyrosine kinase inhibitor. T are mainstay of BC treatment. The side-effects seen with T in combination with gefitinib and erlotinib include neutropenia, diarrhea and rash. Based on preclinical synergy, early clinical studies with L and paclitaxel (P) or docetaxel (D) were studied. Methods: We summarize pharmacokinetics (PK) and preliminary safety data from 192 patients. Results: PK analysis for EGF10009 (q3w), show systemic exposure was increased for both L (21%) and P (23%) at doses of 1500mg daily and 175mg/m2/q3w, respectively. PK analysis in EGF10021 , (L 1250 mg & D 75 mg/m2 with prophylactic pegfilgrastim) indicated no significant effect on systemic exposure of either agent. Toxicities across all studies include i.e., for all patients = grade 3, neutropenia (7.3%), diarrhea (18.2%), rash (3.6%). The rate of adverse events for neutropenia and rash were similar to each agent alone, however diarrhea was more common. The frequency and severity of diarrhea was increased in studies EGF10009 and EGF102580 where no proactive treatment of diarrhea was introduced, whereas in EGF105764, with proactive treatment, currently no =grade 3 diarrhea has been reported. The data show that the combination of L and P has clinical activity (>70% RR reported in EGF102580). Conclusions: T plus L combinations have a predictable and manageable safety profile and clinical activity of P plus L combination was observed. Proactive diarrhea management is essential for these combinations. Based on the PK data, no dose adjustments are required, and any dose adjustments should be toxicity-based. Ongoing clinical studies investigating the combinations of L with T, and combinations of L with T plus trastuzumab will be reported in the future. [Table: see text] No significant financial relationships to disclose.

The first-in-class anti-cancer agent ABTL0812 is effective in preclinical models of human endometrial cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e17070-e17070
Author(s):  
Eva Colàs Colàs ◽  
Nuria Eritja ◽  
Pau Muñoz-Guardiola ◽  
Sonia Sole-Sanchez ◽  
Cristian Moiola ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Endometrial Cancer ◽  
Mouse Model ◽  
Endometrial Adenocarcinoma ◽  
Preclinical Models ◽  
Phase Ib ◽  
Anti Cancer ◽  
Ishikawa Cells ◽  
Cancer Agent

e17070 Background: ABTL0812 is a first-in-class anti-cancer agent with a unique mechanism of action currently in Phase Ib/IIa clinical development for endometrial cancer and squamous NSCLC. ABTL0812 successfully culminated a Phase I clinical trial showing a high safety profile and long disease stabilizations, including 14-months stabilization in a patient with platinum-unresponsive Grade IIIC endometrial cancer with mutated PI3KCA and Akt. Methods: ABTL0812 synergy with paclitaxel and carboplatin was tested in vitro on Ishikawa cells by MTT assay. ABTL0812 in vivo anti-tumor activity was assessed in a PTEN-null inducible mouse model of endometrial adenocarcinoma development upon tamoxifen injection. In vivo synergy between ABTL0812 and paclitaxel was validated in a xenograft model orthotopically implanted with Ishikawa cells and between ABTL0812 and paclitaxel/carboplatin (P/C) in xenografts derived from a patient (PDX) with grade IIIC2 endometrial carcinoma with mutated PI3KCA. Results: ABTL0812 reduced paclitaxel and carboplatin IC50 by 1.5 and 2.1 times respectively in Ishikawa cells. Synergy with paclitaxel was found in Ishikawa orthoxenografts, showing a maximum Tumor Growth Inhibition (maxTGI) of 56,7±16,9% compared with 34.6±33.2% of paclitaxel group. ABTL0812 alone was effective reducing endometrial intraepithelial neoplasia formation in a mouse model of endometrial adenocarcinoma. Additionally, in an endometrial cancer PDX, ABTL0812 alone showed similar efficacy with reduced toxicity when compared with P/C and improved maxTGI when given in combination (ABTL0812: 45,2±17,5%; C/P*: 38,7±26,9%; ABTL0812+C/P*: 59.3±8.8%; *p=0.031). Conclusions: ABTL0812 has shown efficacy as a single agent and in combination with chemotherapy in preclinical models of endometrial cancer with mutations on PI3K/Akt pathway, which appears frequently over-activated in patients with these cancers. These results supported the application of ABTL0812 as a first line therapy in combination with chemotherapy for the Phase Ib/IIa clinical trial currently ongoing, positioning ABTL0812 as a potential therapeutic agent in the treatment of endometrial cancers bearing these genetic alterations.

Safety profile of avelumab in patients with advanced solid tumors: A JAVELIN pooled analysis of phase 1 and 2 data.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 3059-3059 ◽  
Author(s):  
Karen Kelly ◽  
Jeffrey R. Infante ◽  
Matthew H. Taylor ◽  
Manish R. Patel ◽  
Michael S. Gordon ◽  
...  
Keyword(s):  
Adverse Events ◽  
Safety Profile ◽  
Phase 1 ◽  
Safety Data ◽  
Pooled Analysis ◽  
Clinical Activity ◽  
Thyroid Disorder ◽  
Phase 2 ◽  
Phase 2 Trial ◽  
Grade 3

3059 Background: Avelumab is a fully human IgG1 anti–PD-L1 antibody with clinical activity in several tumor types. Pooled safety data from a large phase 1 trial in various tumors and a phase 2 trial in Merkel cell carcinoma (NCT01772004, NCT02155647) were analyzed to further characterize the safety profile of avelumab. Methods: Patients (pts) received avelumab 10 mg/kg 1-hour IV Q2W until progression, unacceptable toxicity, or withdrawal. Treatment-related adverse events (TRAEs) were graded by NCI CTCAE. In post hoc analyses, immune-related adverse events (irAEs) were identified via an expanded AE list and medical review, and infusion-related reaction (IRR) events were identified based on prespecified MedDRA terms, occurring within 1 day or related symptoms that resolved within 2 days of infusion. Results: In 1,738 pts analyzed (phase 1, n = 1,650; phase 2, n = 88) who received ≥1 dose of avelumab for a median of 12 weeks (range 2-138), the most common any grade TRAEs were fatigue (n = 307, 18%), IRR (n = 295, 17%), and nausea (n = 150, 9%). 177 pts (10%) had a grade ≥3 TRAE; most common were fatigue and elevated lipase (17 [1%] each). TRAEs led to discontinuation in 107 pts (6%). Four pts (0.2%) died due to a TRAE. Any grade irAEs occurred in 247 pts (14%), which were grade ≥3 in 39 pts (2%) and considered serious in 43 pts (2%). The most common any grade irAEs were thyroid disorder (n = 98, 6%) and rash (n = 90, 5%). Other irAEs (eg, colitis, hepatitis, pneumonitis, adrenal insufficiency, myositis) each occurred in < 2%. irAEs led to discontinuation in 34 pts (2%). IRR or related symptoms (eg, chills, pyrexia, hypersensitivity) occurred in 439 pts (25%), which were grade 3 in 9 pts (0.5%) and grade 4 in 3 pts (0.2%). An IRR occurred at first infusion in 79% and within first 4 doses in 99%; 63/439 pts (14%) had IRR recurrence in later cycles. IRR led to dose interruption in 152 (9%), infusion rate reduction in 124 (7%), and discontinuation in 35 pts (2%). Conclusions: This large pooled analysis confirms that avelumab has an acceptable safety profile. A minority of pts experienced a grade ≥3 TRAE or irAE and discontinuation due to TRAEs was uncommon. IRRs mostly occurred at first infusion and the rate of recurrence was low. Clinical trial information: NCT01772004, NCT02155647.

scholarly journals Metformin: The Answer to Cancer in a Flower? Current Knowledge and Future Prospects of Metformin as an Anti-Cancer Agent in Breast Cancer

Biomolecules ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 846 ◽  
Author(s):  
Samson Samuel ◽  
Elizabeth Varghese ◽  
Peter Kubatka ◽  
Chris Triggle ◽  
Dietrich Büsselberg
Keyword(s):  
Breast Cancer ◽  
Clinical Studies ◽  
Current Knowledge ◽  
Chemotherapeutic Agents ◽  
Cancer Drug ◽  
Rapid Progression ◽  
Future Prospects ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Tumor Agent

Interest has grown in studying the possible use of well-known anti-diabetic drugs as anti-cancer agents individually or in combination with, frequently used, chemotherapeutic agents and/or radiation, owing to the fact that diabetes heightens the risk, incidence, and rapid progression of cancers, including breast cancer, in an individual. In this regard, metformin (1, 1-dimethylbiguanide), well known as ‘Glucophage’ among diabetics, was reported to be cancer preventive while also being a potent anti-proliferative and anti-cancer agent. While meta-analysis studies reported a lower risk and incidence of breast cancer among diabetic individuals on a metformin treatment regimen, several in vitro, pre-clinical, and clinical studies reported the efficacy of using metformin individually as an anti-cancer/anti-tumor agent or in combination with chemotherapeutic drugs or radiation in the treatment of different forms of breast cancer. However, unanswered questions remain with regards to areas such as cancer treatment specific therapeutic dosing of metformin, specificity to cancer cells at high concentrations, resistance to metformin therapy, efficacy of combinatory therapeutic approaches, post-therapeutic relapse of the disease, and efficacy in cancer prevention in non-diabetic individuals. In the current article, we discuss the biology of metformin and its molecular mechanism of action, the existing cellular, pre-clinical, and clinical studies that have tested the anti-tumor potential of metformin as a potential anti-cancer/anti-tumor agent in breast cancer therapy, and outline the future prospects and directions for a better understanding and re-purposing of metformin as an anti-cancer drug in the treatment of breast cancer.

Safety and clinical activity of first-line durvalumab in advanced NSCLC: Updated results from a Phase 1/2 study.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e20504-e20504 ◽  
Author(s):  
Scott Joseph Antonia ◽  
Julie R. Brahmer ◽  
Ani Sarkis Balmanoukian ◽  
Dong-Wan Kim ◽  
Sang-We Kim ◽  
...  
Keyword(s):  
Safety Profile ◽  
Phase 1 ◽  
Single Agent ◽  
Safety Data ◽  
Clinical Activity ◽  
First Line ◽  
Tumor Biopsy ◽  
Treatment Naïve ◽  
Grade 3 ◽  
Ecog Ps

e20504 Background: Single-agent durvalumab demonstrated manageable safety and encouraging clinical activity in advanced squamous and non-squamous NSCLC in preliminary analyses from the Phase 1/2 1108 study (NCT01693562). Here we present updated safety data and clinical activity in NSCLC pts with no prior treatment for advanced disease. Methods: In this Phase 1/2 dose-escalation and expansion study, pts with Stage IIIB/IV NSCLC, ECOG PS 0–1, and availability of a fresh tumor biopsy and/or archival tumor tissue for PD-L1 testing received durvalumab 10 mg/kg every 2 weeks for up to 12 months, with retreatment permitted for those progressing after 12 months of therapy. Tumor PD-L1 expression was assessed using the Ventana PD-L1 (SP263) Assay (PD-L1 high: ≥25% of tumor cells with membrane staining). Results: As of 24 October 2016, 59 pts (63% ECOG PS 1, 49% squamous) received first-line durvalumab. Median duration of follow-up was 17.3 (1.0–36.8) mos. Safety profile was consistent with the overall (N = 304, ≥0 prior lines of therapy) NSCLC cohort. All-grade treatment-related adverse events (AEs) were reported in 56%; the most common were fatigue (15%), diarrhea (13%), and decreased appetite (10%). 7% had a treatment-related AE leading to discontinuation of durvalumab, including diarrhea in 2 pts. Grade ≥3 treatment-related AEs (all n = 1) occurred in 10%; 1 pt died due to drug-related pneumonia. 49 pts had high PD-L1 expression and 9 pts had low/negative PD-L1 expression; data are not summarized for the latter group due to the small number of pts. For the PD-L1 high subpopulation, confirmed ORR (investigator-assessed RECIST v1.1) was 28.6% (95% CI 16.6–43.3) and disease control rate (stable disease ≥24 weeks) was 42.9% (95% CI 28.8–57.8); median PFS was 4.0 months (95% CI 2.3–9.1), median OS was 21.0 months (95% CI 14.5–not estimable), and 12-month OS rate was 72% (95% CI 56–83). Response rates were similar and durable regardless of histology. Conclusions: Consistent with prior data, durvalumab had a tolerable safety profile in advanced treatment-naïve NSCLC. Clinical activity was seen in PD-L1 high pts, with encouraging OS. Clinical trial information: NCT01693562.

Benzoxazinoids in human diet: an anti-cancer agent?

2019 ◽  
Author(s):  
B Bhattarai ◽  
SK Steffensen ◽  
PL Gregersen ◽  
JH Jensen ◽  
KD Sørensen ◽  
...  
Keyword(s):  
Human Diet ◽  
Anti Cancer ◽  
Cancer Agent
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