Pilot feasibility randomised sham-controlled trial of electroacupuncture for taxane-induced peripheral neuropathy in Breast Cancer patients during treatment

Start Date02 Jun 2022

Sponsor / Collaborator-

NCT04760431

/ Not yet recruitingPhase 2IIT

Anti-HER2 TKI Versus Pertuzumab in Combination With Dose-dense Trastuzumab and Taxane as First Line in HER2-positive Breast Cancer Patients With Active Brain Metastases: A Phase II, Multicenter, Double-blind, Randomized Clinical Trial

This is a prospective, randomized, 2-arm, Phrase 2, superiority and multicenter study to compare the efficiency of Anti-HER2 TKI versus Pertuzumab in Combination With Dose-dense Trastuzumab and Taxane in HER2-positive breast cancer patients with active refractory brain metastases.

Start Date01 Oct 2021

Sponsor / Collaborator

Second Affiliated Hospital Zhejiang University College of

[+2]

100 Clinical Results associated with Proliposomal Intravesical Paclitaxel

100 Translational Medicine associated with Proliposomal Intravesical Paclitaxel

100 Patents (Medical) associated with Proliposomal Intravesical Paclitaxel

40,313

Literatures (Medical) associated with Proliposomal Intravesical Paclitaxel

16 Mar 2025·JOURNAL OF DRUG TARGETING

Reversal potentials of Tween 20 in ABC transporter-mediated multidrug-resistant cancer and treatment-resistant depression through interacting with both drug-binding and ATP-binding areas on MDR proteins

Article

Author: Huang, Yu-Hsin ; Chiu, Wen-Chin ; Teng, Yu-Ning ; Ho, Yu-Cheng ; Chen, Jing-Yi

Drug efflux transporters, especially those belonging to the ATP-binding cassette (ABC) transporter superfamily, play a crucial role in various drug resistance issues, including multidrug resistance (MDR) in cancer and treatment-resistant depression (TRD) in individuals with major depressive disorder. Key transporters in this context include P-glycoprotein (P-gp), multidrug resistance protein 1 (MRP1), and breast cancer resistance protein (BCRP). This study aimed to investigate the modulatory effects of polyoxyethylene (20) sorbitan monolaurate (Tween 20) on these efflux transporters in vitro and to evaluate its potential for overcoming drug resistance in two models: an in vitro cancer MDR model and an in vivo TRD model. The findings indicated that 0.001% Tween 20 significantly inhibited the efflux actions of all three transporters. Additionally, 0.005% Tween 20 effectively reversed resistance to paclitaxel, vincristine, doxorubicin, and mitoxantrone in various cancer MDR cell lines. In the in vivo depression-like behaviour model, 0.01% Tween 20 markedly enhanced the antidepressant and anxiolytic effects of fluoxetine. Given its strong inhibitory effects on P-gp, MRP1, and BCRP, along with its capacity to reverse drug resistance both in vitro and in vivo, Tween 20 is a compelling candidate for tackling transporter-mediated drug resistance.

01 Mar 2025·SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY

Wash-free and ultra-low concentration monitor lysosomal viscosity in apoptosis with a noteworthy fluorescent probe

Article

Author: Wei, Mengmeng ; Han, Zhida ; Li, Chuanya ; Wu, Yukun ; Yang, Rui ; Gao, Qinyi ; Zhu, Changxin ; Lu, Xue

The visualization and subsequent monitoring of apoptosis holds paramount significance in the domains of physiology, pathology, and pharmacology. However, traditional probes require high staining concentrations and multiple washing steps, which would alter the specimen's micro-environment, potentially inducing harm to specimen. To overcome these challenging issues, we have rationally designed and prepared a pH-inert lysosomal probe (named IVTI) to wash-free visualize apoptosis with ultra-low concentration to alleviate the disturbance of probe concentration, washing procedure and pH variations. Compared with general lysosomal probes, IVTI showed a significant fluorescence boost in reflex to elevated viscosity, while its fluorescence intensity remained mostly still when altering pH values, which could achieve more accurate visualization of lysosomes. Moreover, the probe can detect minute viscosity fluctuations in lysosomes under extra-low concentration, greatly eliminating the effect of probe concentration and washing steps to live bio-samples. Furthermore, compared to LTR (Lyso-Tracker Red, a commercial lysosome probe), IVTI offered exceptional imaging capabilities, and the fluorescence images of IVTI was still clear when lysosomal pH increased, which attributed to the pH-inert properties of IVTI. In view of the excellent imaging abilities, the pH-inert probe was applied to in-situ and real time visualize viscosity changes of live cells under extra-low concentration without washing procedure, and the increase of lysosomal viscosity during apoptosis was also monitored by the probe, thereby minimizing the disturbance of probe concentration, washing procedure and pH variations during apoptosis. The probe possesses tremendous potential in the visualization of dynamic changes related to lysosomes in various physiological processes.

01 Mar 2025·Drug Delivery and Translational Research

Combination therapy using Cel-CSO/Taxol NPs for reversing drug resistance in breast cancer through inhibiting PI3K/AKT/NF-κB/HIF-1α pathway

Article

Author: Zeng, Huahui ; Wang, Guoqiang ; Wang, Can ; Li, Xiaofang ; Zhang, Zhenqiang ; Tian, Qikang ; Luo, Ying ; Zeng, Xiaohu ; Zhao, Junwei ; Peng, Haotian ; Zhao, Lingzhou ; Li, Ruiqin ; Wu, Xiangxiang

The resistance of malignant tumors to multiple drugs is a significant obstacle in cancer treatment and prognosis. Accordingly, we synthesized a celastrol (Cel) prodrug (Cel-CSO) by conjugating chitosan oligosaccharides (CSO) to Cel for reversing Taxol resistance in chemotherapy, followed by self-assembly with Taxol into a novel nanoplatform of Cel-CSO/Taxol nanoparticles (termed NPs). NPs showed a suitable size (about 153 nm), excellent stability and prolonged release of Cel and Taxol in a manner that depended on both pH and time. NPs effectively inhibited the overexpression of multidrug resistance-related protein P-gp, hypoxia inducible factor-1α (HIF-1α), and triggered the MCF-7/Taxol cell apoptosis through inhibiting the PI3K/AKT/NF-κB/HIF-1α pathway. In tumor-bearing mice, NPs exhibited significant curative effects in inducing apoptosis of MCF-7/Taxol tumors which showed a low expression level of P-gp, microtubule-related proteins TUBB3 and Tau. The results indicated that NPs may be a promising strategy to overcome drug resistance caused by P-gp, which improve the antitumor effects in drug-resistant breast cancer.

News (Medical) associated with Proliposomal Intravesical Paclitaxel

08 Apr 2024

·www.biospace.com

Boundless Bio Presents Preclinical and Clinical Pharmacodynamic Data on its Lead Extrachromosomal DNA (ecDNA)-Directed Therapy, BBI-355, at the American Association for Cancer Research Annual Meeting 2024

Findings support the ongoing development of BBI-355, a novel, oral, selective inhibitor of checkpoint kinase 1 (CHK1) in Phase 1/2 development, as a differentiated treatment approach for ecDNA-enabled oncogene amplified cancers Third poster presentation to highlight the potential role of ecDNA-based resistance to chemotherapy SAN DIEGO--(BUSINESS WIRE)-- Boundless Bio (Nasdaq: BOLD), a clinical-stage oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, presents preclinical and clinical pharmacodynamic data on its lead ecDNA-directed therapy (ecDTx), BBI-355, and research on ecDNA-mediated acquired resistance to chemotherapy at the American Association for Cancer Research (AACR) Annual Meeting 2024. BBI-355 is a novel, oral, selective inhibitor of checkpoint kinase 1 (CHK1) being studied in the ongoing, first-in-human, Phase 1/2 POTENTIATE clinical trial in patients with oncogene amplified cancers. “Extrachromosomal DNA afford unique advantages to tumors, typically rendering existing therapies ineffective and correlating with poor patient outcomes,” said Chris Hassig, Ph.D., Chief Scientific Officer of Boundless Bio. “Our first poster presented this year at AACR demonstrated that BBI-355 overcame ecDNA-mediated targeted therapy resistance in preclinical tumor models by leveraging the enhanced reliance of ecDNA-driven tumor cells on CHK1 for survival. BBI-355 showed substantial antitumor activity, including complete and durable regressions, in preclinical oncogene amplified models. Dr. Hassig continued, “Today we present preclinical and preliminary clinical pharmacodynamic biomarker assay data that showed detection of CHK1 inhibition-associated replication stress in both patient skin and tumor tissue following administration of BBI-355. In addition, we report a possible role for ecDNA in acquired resistance to chemotherapy observed in preclinical models, extending the potential applicability of ecDNA-directed strategies beyond targeted therapy resistance. We are encouraged by these findings as we continue to advance BBI-355 through the ongoing Phase 1/2 POTENTIATE clinical trial.” Details of the presentations are as follows: Title: Oral CHK1 inhibitor BBI-355 allows flexibility of dose and schedule with demonstration of monotherapy and combinational antitumor activity in extrachromosomal DNA (ecDNA)-driven oncogene amplified preclinical models Abstract Number: 613 Session Category: Experimental and Molecular Therapeutics Session Title: Kinase and Phosphatase Inhibitors 1 Session Date and Time: Sunday Apr 7, 2024, 1:30 PM – 5:00 PM PT Location: Poster Section 25 Poster Board Number: 23 BBI-355 showed inhibition of CHK1 in a host of tumor cell lines and demonstrated in vivo single agent tumor growth inhibition, including complete tumor regressions, across a range of tumor models representing multiple different oncogene amplifications and tumor types. BBI-355 also demonstrated synergistic tumor growth inhibition, including durable regressions, when combined with targeted therapies across multiple oncogene amplified tumor models. Title: Preclinical and clinical pharmacodynamic characterization of BBI-355, a novel, orally bioavailable, and selective CHK1 inhibitor being evaluated in the first-in-human Phase 1/2 POTENTIATE clinical trial of patients with cancer harboring oncogene amplifications Number: 3631 Session Category: Clinical Research Session Title: Biomarkers in Clinical Trials Session Date and Time: Monday Apr 8, 2024, 1:30 PM - 5:00 PM PT Location: Poster Section 40 Poster Board Number: 9 Historically, clinical CHK1 inhibitor programs have lacked effective clinical PD biomarker assays. The findings showed that phosphorylated-CHK1 Ser345 (pCHK1-S345) is a useful pharmacodynamic (PD) biomarker for confirming clinical on-target activity of BBI-355 and could potentially inform the pharmacologically active range of BBI-355 in clinical development. In addition to preclinical data, increased pCHK1-S345 expression by immunohistochemistry in skin biopsies from patients treated with BBI-355 in the ongoing POTENTIATE clinical study were also observed, marking the first, real-time analysis of PD activity from a CHK1 inhibitor in humans. Title: Extrachromosomal DNA (ecDNA) amplification of multi-drug resistance genes results in acquired resistance to taxane-based chemotherapy Abstract Number: 5870 Session Category: Experimental and Molecular Therapeutics Session Title: Mechanisms of Drug Resistance 3 Session Date and Time: Tuesday Apr 9, 2024, 1:30 PM - 5:00 PM PT Location: Poster Section 24 Poster Board Number: 14 Early insights into the role of ecDNA in driving resistance to paclitaxel, a taxane chemotherapy, are revealed and highlight the importance of ecDNA-directed therapies as a potential treatment option for many patients that have chemotherapy-resistant disease. Chemotherapy remains standard of care for many cancer patients, however, resistance to chemotherapy often develops and has been associated with the emergence of multi-drug resistance (MDR) gene amplification, such as ABCB1. These preclinical findings showed that ecDNA-enabled MDR gene amplification can cause short-and long-term resistance to paclitaxel, potentially driving resistance to chemotherapy in patients and underscoring the broad need for ecDTx for chemotherapy-resistant patient populations. About BBI-355 Boundless Bio’s lead ecDNA-directed therapy (ecDTx), BBI-355, is a novel, oral, selective inhibitor of checkpoint kinase 1 (CHK1) being studied in the ongoing, first-in-human, Phase 1/2 POTENTIATE clinical trial (NCT05827614) in patients with oncogene amplified cancers. CHK1 is a master regulator of cells’ response to replication stress (RS). RS is elevated in ecDNA-enabled oncogene amplified cancer cells and, because of this, represents a key vulnerability of those cells. BBI-355 was designed to exploit the elevated RS in ecDNA-enabled oncogene amplified cancer cells by disrupting proper CHK1 function in regulating RS and thereby facilitating catastrophic RS to preferentially kill cancer cells relative to healthy cells. About Boundless Bio Boundless Bio is a clinical-stage oncology company dedicated to unlocking a new paradigm in cancer therapeutics to address the significant unmet need of patients with oncogene amplified tumors by targeting extrachromosomal DNA (ecDNA), a root cause of oncogene amplification and observed in more than 14% of cancer patients. Boundless Bio is developing the first ecDNA-directed therapy (ecDTx), BBI-355, which is an oral inhibitor of checkpoint kinase 1 (CHK1) and is being evaluated in a Phase 1/2 clinical trial in patients with oncogene amplified cancers. Boundless Bio’s second ecDTx, BBI-825, is an oral inhibitor of ribonucleotide reductase (RNR) and recently entered a Phase 1/2 clinical trial in cancer patients with resistance gene amplifications. Leveraging its Spyglass platform, Boundless Bio has additional programs advancing through preclinical development and discovery. Boundless Bio is headquartered in San Diego, CA. For more information, visit . Follow us on LinkedIn and Twitter. Forward-Looking Statements Boundless Bio cautions you that statements contained in this press release regarding matters that are not historical facts are forward-looking statements. The forward-looking statements are based on our current beliefs and expectations and include, but are not limited to: the potential therapeutic benefits of our ecDTx in treating patients with oncogene amplified cancers; and the possibility to extend potential applicability of ecDTx beyond targeted therapy resistance. Actual results may differ from those set forth in this press release due to the risks and uncertainties inherent in our business, including, without limitation: we are early in our development efforts and our approach to discover and develop ecDTx directed against ecDNA in oncogene amplified cancers is novel and unproven; results from preclinical studies or early clinical trials not necessarily being predictive of future results; potential delays in the commencement, enrollment, data readouts or completion of clinical trials or preclinical studies; our dependence on third parties in connection with clinical trials, preclinical studies, ecDNA diagnostic development, and manufacturing; unfavorable results from clinical trials or preclinical studies; unexpected adverse side effects or inadequate efficacy of our ecDTx that may limit their development, regulatory approval, and/or commercialization; regulatory developments in the United States and foreign countries; and other risks described in our filings with the Securities and Exchange Commission (SEC), including under the heading “Risk Factors” in the final prospectus dated March 27, 2024 that we filed with the SEC and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and we undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995.

Clinical StudyAACR

04 Apr 2024

·firstwordpharma.com

Novartis aims for broader Pluvicto use after prostate cancer study update

Novartis confirmed plans Thursday to file for a label expansion of its radioligand drug Pluvicto (lutetium 177 vipivotide tetraxetan) in the second half of 2024, aiming to secure approval for its use in advanced prostate cancer patients prior to treatment with taxane-based chemotherapy.The regulatory submission will be based on updated results from the Phase III PSMAfore study, which evaluated Pluvicto in patients with PSMA-positive metastatic castration-resistant prostate cancer (mCRPC) after treatment with androgen receptor pathway inhibitors (ARPI).OS prompted previous delayIn findings from the second interim analysis of PSMAfore with 45% of events, unveiled last October at the European Society for Medical Oncology (ESMO) congress, Pluvicto demonstrated a 59% benefit on the primary endpoint of radiographic progression-free survival (rPFS) compared to daily oral androgen therapy.However, the study's design allowed control patients to receive Pluvicto at disease progression – something that muddied up the interpretation of overall survival (OS) data given the exceptionally high 84% rate of treatment crossover. At the time, Novartis said Pluvicto was associated with a 16% higher risk of death before adjusting for crossover; but when crossover events were taken into account, the drug exhibited a 20% decrease in mortality risk.Nevertheless, questions about the OS data prompted Novartis to postpone its projected timeline for seeking a broader US label from the third quarter of 2023 to sometime this year. For more, see – KOL Views Q&A: PSMAfore not a win for Pluvicto but Novartis still has path to growth in CRPC.HR of less than 1.0On Thursday, Novartis said that "at approximately 75% of the targeted information fraction for the trial's primary endpoint of rPFS, Pluvicto demonstrated a hazard ratio (HR) of less than 1.0 compared to an alternative ARPI in the intent-to-treat population, unadjusted for crossover to Pluvicto treatment."Novartis stated that rPFS and other secondary efficacy endpoints were "consistent" with interim results presented in 2023, while an additional eight months of follow-up data revealed no new safety concerns. Full results will be shared at an upcoming medical meeting.Pluvicto is already approved in the US for patients with PSMA-positive mCRPC who have been treated with ARPI and taxane-based chemotherapy. The radiopharmaceutical became Novartis' fastest-growing drug in 2023 with sales more than tripling to $980 million.

Clinical ResultPhase 3Drug Approval

08 Mar 2024

·www.businesswire.com

Agendia Presents Data at Miami Breast 2024 Demonstrating MammaPrint® + BluePrint®’s Ability to Further Stratify Tumor Categories in Hormone-Positive Breast Cancer, Highlighting Response to Different Chemotherapy Regimens

IRVINE, Calif. & AMSTERDAM--( BUSINESS WIRE )-- Agendia ® , Inc. , announced today it will share new data from the ongoing prospective, observational FLEX Trial ( NCT03053193 ) in two poster presentations at the 41 st Annual Miami Breast Cancer Conference (MBCC), taking place March 7 – 10 th , 2024. The first poster, titled MammaPrint ® and BluePrint ® predict anthracycline chemosensitivity in patients with HR+HER2-early-stage breast cancer enrolled in FLEX, (Audeh, W., et al.), investigates the associations between MammaPrint and BluePrint classifications, therapy regimen, and the likelihood of achieving a pathologic Complete Response (pCR). Researchers looked at patients who had hormone receptor-positive (HR+), Human Epidermal Growth Factor Receptor (HER) 2-negative early-stage breast cancer – categorized as MammaPrint High Risk – who had been treated with either a combination of two (taxane and cyclophosphamide, TC) or three (TC with anthracycline, AC-T) types of neoadjuvant chemotherapy. Patients were then further stratified into MP High 1 and High 2 categories, and further stratified by BluePrint subtype of Luminal and Basal. Results showed that patients with MP High 2 tumors, including Luminal B and Basal subtypes, are more likely to achieve a pCR in response to AC-T, while the addition of anthracycline to the therapy regimen does not appear to improve pCR rates for patients with MP High 1, Luminal B-type tumors. The second poster, titled Prediction of chemotherapy benefit by MammaPrint ® in patients with HR+HER2-early-stage breast cancer from real-world evidence studies (Audeh, W., et al.), used data from patients with HR+ HER2-negative early-stage breast cancer enrolled in the FLEX and NBRST trials to generate a prediction of the magnitude of chemotherapy benefit based upon a patient’s genomic risk, looking at the MammaPrint index more closely as a continuous variable. Researchers examined the association of the MammaPrint index with benefit from chemotherapy by evaluating two clinical endpoints, the likelihood of pCR in response to neoadjuvant chemotherapy, and the five-year outcome among patients who received chemotherapy and endocrine therapy or endocrine therapy alone. Consistent with results found in the landmark MINDACT trial, this study showed that the MammaPrint index demonstrates strong efficacy in predicting low chemosensitivity in Low Risk and Ultra Low Risk tumors, reinforcing that these groups do not derive significant chemotherapy benefit. However, it was also observed that chemotherapy effectiveness increased as MammaPrint risk increased in High 1 and High 2 tumors, as evidenced by both pCR rates and 5-year outcomes, demonstrating that the overall benefit of chemotherapy increases as MammaPrint risk increases. Taken together, these findings indicate the utility of MammaPrint to predict neoadjuvant and adjuvant chemotherapy benefit in this patient population. “In this unique real world evidence FLEX study, we were able to look at chemosensitivity for patients who had received neoadjuvant treatment and the chemo benefit for patients who are treated with systemic therapy after surgery, showing that MammaPrint is predictive of chemotherapy benefit in both cases. The FLEX Trial, with over 16,000 women enrolled, is now allowing us to look at clinical outcomes as well as analyzing whole transcriptome data,” said William Audeh, MD, MS, Chief Medical Officer of Agendia. “The data we’re sharing at the Miami Breast Cancer Conference confirms that gene expression profiling with these assays identify who may benefit from chemotherapy, and may prove helpful in regimen selection as well. We look forward to further exploring the capabilities of MammaPrint and BluePrint for women across the entire spectrum of breast cancer risk and subtype.” The goal of Agendia’s research is to increase the likelihood of managing each individual’s cancer diagnosis by delivering a customized treatment plan to the patients most likely to benefit based on the unique features of their tumor. About Agendia Agendia is a leading provider of innovative solutions in the field of precision oncology. With a focus on early-stage breast cancer, Agendia offers reliable biological insights that inform personalized treatment decisions for patients and their care teams. Their advanced genomic assays, MammaPrint ® + BluePrint ® , enable clinicians to quickly identify the most effective treatment plan, minimizing the risk of both under- and over-treatment. Founded in 2003 in Amsterdam, Agendia is headquartered in Irvine, California with a state-of-the-art laboratory facility. Led by world-renowned scientists and oncologists, Agendia is committed to advancing genomic insights through ongoing research. This includes the notable FLEX Study– the world's largest whole transcriptome Real-World Evidence-based Breast Cancer database which aims to revolutionize precision in breast cancer management. With cutting-edge technology, research and innovation, Agendia strives to shape the future of precision oncology and make a significant impact in the fight against breast cancer. About MammaPrint MammaPrint ® is a gene expression profiling test that reveals the distinct underlying biology of an early-stage tumor to determine its risk of spreading. As the only FDA-cleared gene expression profiling test to assess a woman's risk of distant metastasis, MammaPrint ® provides critical answers that help inform the future of her treatment plan at the point of diagnosis, including the timing and benefit to chemotherapy and endocrine therapy. MammaPrint® listens to the signals from 70 key genes in a woman’s tumor to stratify her risk within four distinct categories - ranging from UltraLow, Low, High 1, and High 2– to fuel a right-sized care plan tailored to her biology and her life's plans. About BluePrint BluePrint ® is a gene expression profiling test that reveals the driving forces behind a tumor’s growth at the earliest stage possible in a woman’s breast cancer care journey to help optimize and personalize treatment planning. As the only molecular subtyping test available in the U.S., BluePrint® goes where pathology cannot, offers critical insights that providers may otherwise have not known to act on, and gives women the best chance to return to a life not defined by cancer. BluePrint® measures the activity of 80 key genes that are involved in a tumor's growth to classify a tumor as Luminal-type, HER2-type, or Basal-type, each of which warrant distinct treatment pathways. By revealing the distinct underlying biology of a woman's tumor, BluePrint® can catch often misclassified, yet highly aggressive, Basal tumors, so women can be prescribed the most appropriate treatment from the start.

Clinical ResultClinical Study

100 Deals associated with Proliposomal Intravesical Paclitaxel

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Indication	Highest Phase	Country/Location	Organization	Date
Non-Muscle Invasive Bladder Neoplasms	Phase 2	US	TesoRx Pharma LLC	17 May 2018
Urothelial Carcinoma of the Urinary Bladder	Phase 2	US	TesoRx Pharma LLC	17 May 2018
Bladder Cancer	Phase 2	-	TesoRx Pharma LLC	-
Malignant Pleural Effusion	Preclinical	US	LIPAC Oncology LLCStartup	11 Jun 2024
Ovarian Cancer	Preclinical	US	LIPAC Oncology LLCStartup	11 Jun 2024
Peritoneal Neoplasms	Preclinical	US	LIPAC Oncology LLCStartup	11 Jun 2024

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ASCO2023	Not Applicable	Recurrent Squamous Cell Carcinoma of the Head and Neck	444	Platinum/5FU/pembrolizumab	xzmfvhszup(liyfhkgrih) = zvfatropac uajcsclpcj (gazzpfkkys ) View more	-	31 May 2023
				Platinum/taxane/pembrolizumab	xzmfvhszup(liyfhkgrih) = wmcpfuflkq uajcsclpcj (gazzpfkkys ) View more
ASCO_GI2023	Not Applicable	Advanced Gastric Adenocarcinoma Third line	73	Taxane plus ramucirumab	wthftbudoo(esqiryaeyg) = jdjtqzocnn cyvjgrhlaz (axbstxmddt ) View more	-	24 Jan 2023
ESMO2022	Not Applicable	Non-Small Cell Lung Cancer Third line	52	Taxanes-based chemotherapy alone	vknuwhqreg(miiwtaqwxn) = zbykwubytf sixasbypkw (epjouhkloc )	Positive	10 Sep 2022
				Taxanes-based chemotherapy plus angiogenesis inhibitors	vknuwhqreg(kxkdyjfaib) = qekxqqhcjf jvpjsobswl (jwwoxzoijh )
ASCO2022	Not Applicable	Squamous Cell Carcinoma of Head and Neck	99	Taxanes + Cetuximab	epptzhqmbr(snkgsqrhws) = nvvbmzwcmq nrgmvgptpm (fzbeixxijf ) View more	-	02 Jun 2022
				Taxanes + Cetuximab + Platinum	fzbcdwsyic(gpsgffthlr) = khdusdywai fbexoyohqj (woqurihfym )
ASCO2020	Not Applicable	Breast Cancer	40	Taxane monotherapy	fpnqchhtiz(xcbboptrzs) = skjeuuhvmv pwftzcpgpa (frtfbuxush )	-	25 May 2020
NCT03081858 (Biospace) Manual	Phase 1/2	Recurrent Bladder Cancer	6	LiPax	vubfkjxczl(thngtiocuv) = bmyvjlzedb lpqhaygrjf (natzolfmpy ) View more	Positive	18 May 2020
ASCO_GU2020	Not Applicable	Metastatic castration-resistant prostate cancer	-	taxanes (High glutamine levels)	wzfltlkujd(iinnhcfjyg) = shnfflmwqd jervrxpnfw (ousshwsytr ) View more	Positive	19 Feb 2020
				taxanes (Low glutamine levels)	wzfltlkujd(iinnhcfjyg) = yoqpkgkqbh jervrxpnfw (ousshwsytr ) View more
ASCO_GU2019	Not Applicable	Penile Neoplasms	-	Taxane combination chemotherapy regimens	gbhoqgokso(taqzivvbcu) = awxfvygioe xmxqpxxmyv (gfcerafrso ) View more	Positive	26 Feb 2019
				Non-taxane regimens	gbhoqgokso(taqzivvbcu) = sdyzfoxopi xmxqpxxmyv (gfcerafrso ) View more
ESMO2018	Not Applicable	Breast Cancer Adjuvant	-	Taxane + Cyclophosphamide combination (TC)	unwiffhdfr(hnmxilvgkw) = piqxadjxex norpereppo (piimmhuixh )	-	22 Oct 2018
				Cyclophosphamide + Anthracycline combination (TaxAC)	unwiffhdfr(hnmxilvgkw) = cjfjxsjgek norpereppo (piimmhuixh )
AACR2017	Not Applicable	Locally advanced breast cancer	63	Chemotherapy based on anthracyclines and taxanes	rptwprhvcm(efamtnvkll) = elkjaeqtvn rvixmsefbm (hogsehcebz )	-	01 Jul 2017

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Proliposomal Intravesical Paclitaxel

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