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

Start Date02 Jun 2022

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100 Clinical Results associated with Proliposomal intravesical paclitaxel

100 Translational Medicine associated with Proliposomal intravesical paclitaxel

100 Patents (Medical) associated with Proliposomal intravesical paclitaxel

Literatures (Medical) associated with Proliposomal intravesical paclitaxel

01 Feb 2022·Nature medicineQ1 · MEDICINE

AAV gene therapy for Tay-Sachs disease

Q1 · MEDICINE

Article

Author: Martin, Douglas R ; Abayazeed, Aly ; Douthwright, Catherine ; Brown, Robert H ; Gounis, Matthew ; Bateman, Scot ; Tai, Phillip W L ; Keeler, Allison M ; Barton, Bruce A ; Vardar, Zeynep ; Blackwood, Meghan ; McKenna-Yasek, Diane ; Mueller, Christian ; Batista, Ana Rita ; Parzych, Julia ; Rohatgi, Saurabh ; Finberg, Robert ; Tifft, Cynthia J ; Moser, Richard ; Gernoux, Gwladys ; Gibson, Laura ; Sena-Esteves, Miguel ; Gray-Edwards, Heather L ; Cataltepe, Oguz ; Spanakis, Spiro G ; Eichler, Florian S ; Flotte, Terence R ; Jiang, Xuntian ; Puri, Ajit ; Shazeeb, Mohammed Salman

Tay-Sachs disease (TSD) is an inherited neurological disorder caused by deficiency of hexosaminidase A (HexA). Here, we describe an adeno-associated virus (AAV) gene therapy expanded-access trial in two patients with infantile TSD (IND 18225) with safety as the primary endpoint and no secondary endpoints. Patient TSD-001 was treated at 30 months with an equimolar mix of AAVrh8-HEXA and AAVrh8-HEXB administered intrathecally (i.t.), with 75% of the total dose (1 × 10¹⁴ vector genomes (vg)) in the cisterna magna and 25% at the thoracolumbar junction. Patient TSD-002 was treated at 7 months by combined bilateral thalamic (1.5 × 10¹² vg per thalamus) and i.t. infusion (3.9 × 10¹³ vg). Both patients were immunosuppressed. Injection procedures were well tolerated, with no vector-related adverse events (AEs) to date. Cerebrospinal fluid (CSF) HexA activity increased from baseline and remained stable in both patients. TSD-002 showed disease stabilization by 3 months after injection with ongoing myelination, a temporary deviation from the natural history of infantile TSD, but disease progression was evident at 6 months after treatment. TSD-001 remains seizure-free at 5 years of age on the same anticonvulsant therapy as before therapy. TSD-002 developed anticonvulsant-responsive seizures at 2 years of age. This study provides early safety and proof-of-concept data in humans for treatment of patients with TSD by AAV gene therapy.

01 May 2016·Anesthesia and analgesiaQ2 · MEDICINE

Proliposomal Ropivacaine Oil: Pharmacokinetic and Pharmacodynamic Data After Subcutaneous Administration in Volunteers

Q2 · MEDICINE

Article

Author: Naveh, Michael ; Ginosar, Yehuda ; Davidson, Elyad M. ; Kagan, Leonid ; Aharon, Arnon ; Haroutounian, Simon

BACKGROUND::

Slow-release liposomal formulations of local anesthetics prolong plasma redistribution and reduce peak plasma drug concentration, allowing safer administration of larger doses and further prolonging sensory effects. However, their clinical applicability is limited by expensive manufacture and liposomal leakage. Previously, we described the simple preparation of a novel proliposomal ropivacaine oil that produces multilamellar liposomal vesicles on exposure to aqueous media and that has a shelf-life of >2 years at room temperature. In this study, we present both pharmacodynamic and pharmacokinetic data in healthy volunteers after subcutaneous injection of this novel proliposomal preparation of ropivacaine.

METHODS::

In the pharmacodynamic phase of this study, 15 volunteers received 3 separate subcutaneous injections of 2.5 mL containing 1 of the following drugs: proliposomal 4% ropivacaine, plain 0.5% ropivacaine, and the ropivacaine-free proliposomal vehicle. Drugs were administered into the lower back, and their location was randomized and blinded; a separate area was used as an uninjected, open control. Experimental sensory assessment was made at repeated intervals over 72 hours using both pinprick sensation and experimental heat pain tolerance (assessed using quantitative sensory testing). In a separate pharmacokinetic phase of this study, 9 volunteers received subcutaneous injections of 2.5 mL of either proliposomal 4% ropivacaine (n = 6) or plain 0.5% ropivacaine (n = 3); these participants had plasma ropivacaine concentrations assessed at repeated intervals over 72 hours.

RESULTS::

The mean ± SE duration of pinprick anesthesia after proliposomal and plain ropivacaine administration lasted 28.8 ± 6.0 and 15.9 ± 3.5 hours, respectively (mean difference, 16.8 hours; 95% confidence interval, 10.0–23.7; P = 0.001). For experimental heat pain, the anesthesia duration was approximately 36 and 12 hours, respectively, with mean ± SE area under the curve of the normalized heat pain tolerance over time 55.0 ± 28.8 Δ°C·min for proliposomal ropivacaine and 9.6 ± 26.0 Δ°C·min for plain ropivacaine (mean difference, 64.6 Δ°C·min; 95% confidence interval, 10.2–119.0; P = 0.036). In the pharmacokinetic study, there was no significant difference in peak plasma concentration in the proliposomal ropivacaine group (164 ± 43 ng/mL compared with 100 ± 41 ng/mL in the plain ropivacaine group; P = 0.07) despite an 8-fold increase in ropivacaine dose in the proliposomal group. The 99% upper prediction limit for peak plasma concentrations (351 ng/mL proliposomal; 279 ng/mL plain) was well below the putative toxic plasma concentration for both groups. The mean ± SE terminal half-life and area under the curve for proliposomal ropivacaine versus plain ropivacaine were 13.8 ± 3.6 hours vs 5.9 ± 2.3 hours (P = 0.011) and 5090 ± 1476 h·ng/mL vs 593 ± 168 h·ng/mL (P = 0.0014), respectively.

CONCLUSIONS::

The prolonged pharmacodynamic effect of proliposomal ropivacaine, together with its delayed elimination and prolonged redistribution to plasma, is compatible to depot-related slow-release and similar to the performance of other liposomal local anesthetics. The advantage of the proliposomal oil is its ease of preparation and its extended shelf-stability at room temperature.

01 Nov 2014·European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical SciencesQ2 · MEDICINE

Proliposomes as a drug delivery system to decrease the hepatic first-pass metabolism: Case study using a model drug

Q2 · MEDICINE

Article

Author: Kadajji, Veeran Gowda ; Issar, Manish ; Venkatesan, Natarajan ; Wang, Zhijun ; Yanamandra, Sarala ; Betageri, Guru V

Objective of the present study was to develop a proliposomal formulation to decrease the hepatic first-pass metabolism of a highly metabolized drug. Lovastatin was chosen as the model drug. Proliposomes were prepared by mixing different ratios of phospholipids such as soy phosphatidylcholine (SPC), hydrogenated egg phosphatidylcholine (HEPC) and dimyristoyl phosphatidylglycerol (DMPG) individually with drug and cholesterol in an organic solvent. Proliposomal powder was obtained following evaporation of the solvent. The proliposomal powder was either filled into capsules or compressed into tablets. Physical characterization, in vitro drug transport studies and in vitro dissolution of formulations and pure drug was carried out. In vitro transport across the membrane was evaluated using parallel artificial membrane permeability assay (PAMPA). The extent of drug released from various proliposomal formulations in the first 30 min was 85%, 87% and 96% with DMPG, SPC and HEPC containing formulations respectively, while the pure drug formulation showed 48% drug release in the same period. In vivo studies were carried out in male Sprague-Dawley rats. Following single oral administration of the selected formulation (F9), a relative bioavailability of 162% was achieved compared to pure lovastatin. The study demonstrated that proliposomes can be used as a drug delivery system to decrease the hepatic first-pass metabolism.

News (Medical) associated with Proliposomal intravesical paclitaxel

24 Apr 2024

·www.pharmaceutical-technology.com

Novartis reports 25% increase in net income in Q1 2024

As of 31 March 2024, Novartis’ net debt stood at $15.8bn. Credit: Michael Derrer Fuchs via Shutterstock. Novartis has reported net income from continuing operations of $2.68bn for the first quarter (Q1) of 2024, marking a 25% increase from $2.15bn in Q1 2023. This growth was primarily attributed to a surge in operating income. Operating income from continuing operations saw a substantial rise to $3.37bn for Q1 2024 from $2.61bn in the previous year’s first quarter, driven by an increase in net sales. The company’s net sales from continuing operations stood at $11.8bn in Q1 2024, an increase from $10.79bn in Q1 2023. Novartis experienced a 24% decrease in free cash flow from continuing operations, which amounted to $2bn, compared to $2.68bn in the same period last year because of a previous-year one-timer and timing of payments. See Also: Novartis gets grant for chimeric antigen receptor for T cell specificity regulation AlphaMedix by Orano Med for Neuroendocrine Gastroenteropancreatic Tumors (GEP-NET): Likelihood of Approval Core operating income showed a 16% increase to $4.5bn, primarily due to the higher net sales while core net income rose by 14% to $3.7bn. As of 31 March 2024, Novartis’ net debt grew to $15.8bn, up from $10.2bn at the end of 2023. This increase was largely due to the $5.2bn annual net dividend payment in March 2023, cash flow for treasury share transactions of $1.1bn, and $1.2bn net cash outflow for mergers and acquisitions, offset partially by the $2bn free cash flow. Looking ahead, Novartis has raised its full-year 2024 guidance, now expecting net sales to grow in the high-single to low double-digit range and core operating income to increase from low double-digit to mid-teens. Novartis CEO Vas Narasimhan said: “Novartis continued our strong momentum with both sales growth and core margin expansion in Q1. “Our performance was broad-based, across all key growth brands and geographies, allowing us to raise guidance for the full year 2024. We continued to advance our pipeline in Q1, with submission-enabling data for Scemblix first-line, Pluvicto pre-taxane and remibrutinib in CSU. The momentum in our business and pipeline gives us continued confidence in our mid- and long-term growth outlook.” Earlier this month, Novartis signed a licence agreement for Arvinas’ ARV-766, a new treatment for prostate cancer

License out/inFinancial StatementPROTACs

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

05 Apr 2024

·www.biospace.com

Novartis to File for Pluvicto Label Expansion After Promising Phase III Data

Pictured: Novartis office in Basel, Switzerland/iStock, Michael Derrer Fuchs Novartis on Thursday announced that it plans to a label expansion for its radioligand therapy Pluvicto (lutetium-177 vipivotide tetraxetan) later this year, proposing to use the prostate cancer treatment in patients who have not yet undergone chemotherapy. The announcement follows additional data from the Phase III PSMAfore study, demonstrating overall survival (OS) data that leaned in favor of Pluvicto. Novartis did not provide specific data in its brief announcement, only revealing that “a pre-planned analysis at approximately 75% information fraction demonstrates an OS hazard ratio less than 1.0” in PSMAfore’s intent-to-treat population, without adjusting for cross-over. Pluvicto’s safety pro the interim analysis remains consistent with what had been previously disclosed in prior readouts, according to the announcement. Novartis will present full findings from PSMAfore at an upcoming medical meeting. Designed to be intravenously administered, Pluvicto is a targeted radioligand therapeutic that works by seeking out the PSMA protein, which is typically found on prostate cancer cells. According to its label, Pluvicto’s active moiety is the radionucleotide lutetium-177, the beta-emissions from which damage the PSMA-positive cancer cells, induce DNA damage and trigger cell death. The FDA signed off on Pluvicto in March 2022, allowing its use in adult patients with metastatic castration-resistant prostate cancer who are positive for the PSMA protein. Currently, Pluvicto can only be administered to those who have been exposed to an androgen receptor pathway inhibitor (ARPI) and taxane-based chemotherapy. Using data from the PSMAfore study, Novartis is seeking to push Pluvicto up into an earlier line of treatment, before taxane therapies. However, in October 2023, the pharma reported that the trial’s OS data were “confounded” by a strong cross-over effect—84% of patients who discontinued ARPI treatment due to radiographic progression transitioned to the Pluvicto arm. Adjusting for cross-overs pointed to a non-significant advantage for Pluvicto, though placebo was better in the unadjusted analysis. Still, PSMAfore met its primary endpoint. The risk of radiographic progression-free survival was 59% lower in the Pluvicto group, compared with simply switching to another ARPI therapy. The radioligand therapy also improved patients’ quality of life, delayed the worsening of their pain and lowered prostate-specific antigen levels. If its label expansion is approved, earlier Pluvicto treatment may help patients avoid the toxic side effects of chemotherapy—and may open a larger market for the targeted treatment. Tristan Manalac is an independent science writer based in Metro Manila, Philippines. Reach out to him on LinkedIn or email him at tristan@tristanmanalac.com or tristan.manalac@biospace.com.

Phase 3Clinical ResultOligonucleotide

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	LIPAC Oncology LLCStartup	17 May 2018
Urothelial Carcinoma of the Urinary Bladder	Phase 2	US	LIPAC Oncology LLCStartup	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

Clinical Result

Indication

Phase

Evaluation

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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/pembrolizumabPlatinum/5FU/pembrolizumab	avyejaexkf(kpdjgdjcjl) = couhsbgeki nlgvsloiil (tenywsdlrr ) View more	-	31 May 2023
				Platinum/taxane/pembrolizumabPlatinum/taxane/pembrolizumab	avyejaexkf(kpdjgdjcjl) = ebadtnwvds nlgvsloiil (tenywsdlrr ) View more
ASCO_GI2023	Not Applicable	Advanced Gastric Adenocarcinoma Third line	73	Taxane plus ramucirumab	fvkebjblyb(anhklogqjc) = dzbojblzxj saxcpysxmg (fbfyisazcl ) View more	-	24 Jan 2023
ESMO2022	Not Applicable	Non-Small Cell Lung Cancer Third line	52	Taxanes-based chemotherapy alone	parwwnfhyv(yjokwoztbe) = lyiuzhkmxo swcfgopzzb (hlbengqwdh )	Positive	10 Sep 2022
				Taxanes-based chemotherapy plus angiogenesis inhibitors	parwwnfhyv(qfpqaspqdc) = udcjcsfrgm naigdhzgzb (twdcmsqtjx )
ASCO2022	Not Applicable	Squamous Cell Carcinoma of Head and Neck	99	Taxanes + Cetuximab	lcnfgntcpt(uqxgpyiwso) = ycmqwrjgbj omngcgrnly (xiyvmswjfc ) View more	-	02 Jun 2022
				Taxanes + Cetuximab + Platinum	teniwgcdde(utkgtnkwue) = jitkxxjpiq ijkkcqdhna (fqqxhursgg )
ASCO2020	Not Applicable	Breast Cancer	40	Taxane monotherapy	cttwvmqvca(hrbzhceuym) = qztmdaefym cqceisbyhw (wssfngbyxt )	-	25 May 2020
NCT03081858 (Biospace) Manual	Phase 1/2	Recurrent Bladder Cancer	6	LiPax	wixyqjderc(oigiearucz) = fwcueurxqb vldawitazv (gwfljrmiwt ) View more	Positive	18 May 2020
ASCO_GU2020	Not Applicable	Metastatic castration-resistant prostate cancer	-	taxanes (High glutamine levels)	dngethsccs(nvwrreovcd) = saopefomra rxggmwvomi (nomiyfecal ) View more	Positive	19 Feb 2020
				taxanes (Low glutamine levels)	dngethsccs(nvwrreovcd) = sgzslibmkm rxggmwvomi (nomiyfecal ) View more
ASCO_GU2019	Not Applicable	Penile Neoplasms	-	Taxane combination chemotherapy regimens	tloeqeslpb(wncqvwadfj) = gqafoxwfnx ihpchykxya (xxkctchtto ) View more	Positive	26 Feb 2019
				Non-taxane regimens	tloeqeslpb(wncqvwadfj) = xzbsnbxsfx ihpchykxya (xxkctchtto ) View more
ESMO2018	Not Applicable	Breast Cancer Adjuvant	-	Taxane + Cyclophosphamide combination (TC)	rtjexluqrb(pxafzpxowj) = vfjmulemfq yhiddgywwi (azowaloioq )	-	22 Oct 2018
				Cyclophosphamide + Anthracycline combination (TaxAC)	rtjexluqrb(pxafzpxowj) = avzkwpuxpb yhiddgywwi (azowaloioq )
FIRSTANA and PROSELICA (Pubmed \| J Urol)	Phase 3	Metastatic castration-resistant prostate cancer First line \| Second line	571	Docetaxel	yfsprzqrba(lwivogrypd): HR = 1.53 (95% CI, 1.18 - 1.97), P-Value = 0.001 View more	-	01 Sep 2018
				Cabazitaxel

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