This trial studies the effect of pegloticase in reducing uric acid levels in patients with hyperuricemia (high blood levels of uric acid) caused by tumor lysis syndrome. Tumor lysis syndrome occurs when the breakdown products of cancer cells, such as uric acid, enter the blood stream. High levels of uric acid in blood may cause kidney damage and reduce kidney function. The goal of this trial is to learn if pegloticase may lower uric acid levels in blood when given to cancer patients with hyperuricemia caused by tumor lysis syndrome.

Start Date05 Apr 2022

Sponsor / Collaborator

The University of Texas MD Anderson Cancer Center

NL-OMON27662 / SuspendedNot Applicable

Treatment of severe gout patients with rasburicase

Start Date03 May 2021

Sponsor / Collaborator-

100 Clinical Results associated with Rasburicase

100 Translational Medicine associated with Rasburicase

100 Patents (Medical) associated with Rasburicase

1,061

Literatures (Medical) associated with Rasburicase

01 Nov 2024·FREE RADICAL BIOLOGY AND MEDICINE

Unconjugated bilirubin promotes uric acid restoration by activating hepatic AMPK pathway

Article

Author: Zhang, Nanxin ; Chen, Xiaojing ; Luo, Jun ; Zhang, Yingqiong ; Li, Ping ; Lin, Nengming ; Chen, Yujia ; Zhang, Bichen ; Li, Qi ; Bai, Mengru ; Jiang, Ting ; Chen, Binxin ; Gao, Yue ; Jiang, Huidi ; Zhou, Hui ; Lu, Shuanghui

Hyperuricemia and its development to gout have reached epidemic proportions. Systemic hyperuricemia is facilitated by elevated activity of xanthine oxidase (XO), the sole source of uric acid in mammals. Here, we aim to investigate the role of bilirubin in maintaining circulating uric acid homeostasis. We observed serum bilirubin concentrations were inversely correlated with uric acid levels in humans with new-onset hyperuricemia and advanced gout in a clinical cohort consisting of 891 participants. We confirmed that bilirubin biosynthesis impairment recapitulated traits of hyperuricemia symptoms, exemplified by raised circulating uric acid levels and accumulated hepatic XO, and exacerbated mouse hyperuricemia development. Bilirubin administration significantly decreased circulating uric acid levels in hyperuricemia-inducing (HUA) mice receiving potassium oxonate (a uricase inhibitor) or fed with a high fructose diet. Finally, we proved that bilirubin ameliorated mouse hyperuricemia by increasing hepatic autophagy, restoring antioxidant defense and normalizing mitochondrial function in a manner dependent on AMPK pathway. Hepatocyte-specific AMPKα knockdown via adeno-associated virus (AAV) 8-TBG-mediated gene delivery compromised the efficacy of bilirubin in HUA mice. Our study demonstrates the deficiency of bilirubin in hyperuricemia progression, and the protective effects exerted by bilirubin against mouse hyperuricemia development, which may potentiate clinical management of hyperuricemia.

01 Oct 2024·Hematology, transfusion and cell therapy

Tumor lysis syndrome in hematological inpatients, experience from a university hospital in Brazil: A retrospective cohort study

Article

Author: Weber, Cristiane Seganfredo ; Calvache, Ebellins Tabares ; Calvache, Allison Dessiret Tabares

INTRODUCTION:

The tumor lysis syndrome is a medical emergency. Its presentation can be spontaneous or secondary, as a consequence of the established treatment. The diagnosis and treatment of the tumor lysis syndrome (TLS) has become a crucial goal to the evolution and improvement of treatments and targeted therapies.

METHODS:

Between January 2014 and December 2019, we retrospectively reviewed inpatients aged over 18 years with hematological neoplasms from a tertiary hospital in Brazil. We identified 112 episodes of TLS in 97 patients. The incidence was 10.5% and the median OS was 13.0 months (95%CI 6.2 - 19.7). The median age was 56 years (IQR 39.5 - 64). The most frequent diagnoses were multiple myeloma (18.6%), acute myeloid leukemia (17.5%) and diffuse large B-cell lymphoma (17.5%). All patients received intravenous (IV) hydration. The management also included the administration of allopurinol in 76% of the cases and rasburicase in eight patients. Renal replacement therapy was necessary in 37% of the cases. In the multivariate analysis, age, HIV status and ICU treatment were significantly associated with OS.

CONCLUSION:

The TLS is a serious complication in the setting of hematological malignancies. The use of scores for risk stratification, as well as the inclusion of prophylactic measures and prompt treatment with frequent laboratory monitoring, is essential to reduce morbidity and mortality in the comprehensive treatment of these patients.

01 Oct 2024·Cancer Reports

Effectiveness of fractionated rituximab in preventing tumor lysis syndrome in aggressive B‐cell lymphoma: Insights from real‐life clinical practice

Article

Author: McKee, Thomas A. ; Lang, Noémie ; Chamuleau, Martine ; Samii, Kaveh ; Mach, Nicolas ; Bouroumeau, Antonin ; Tamburini, Jerome ; Stenner, Frank ; Mohamad, Jasmine

Abstract:

Background:

Tumor lysis syndrome (TLS) is a potentially life‐threatening condition resulting from the rapid destruction of malignant cells, leading to electrolyte imbalances and severe complications, such as acute kidney injury, arrhythmias, and seizures. TLS can be managed through hyperhydration, urate‐lowering treatments, and a steroid prophase strategy.

Aims:

This study aims to explore the impact of fractionated rituximab, an anti‐CD20 antibody, on the occurrence and severity of TLS during the initial cycle in patients with aggressive B‐cell non‐Hodgkin lymphoma (B‐NHL).

Methods:

Data was retrospectively collected from 94 of 186 patients.

Results:

Among the 94 patients included in the analysis, the median age was 70. Histologies were diffuse large B‐cell lymphoma (75%), Burkitt lymphoma (13%) and high‐grade B‐cell lymphoma (8%). The majority were at an advanced stage (93%) with a high IPI score (75%). Most patients received anthracycline‐containing regimens (72%) and prophylactic allopurinol (83%) and/or rasburicase (26%). Steroid prophase was administered to 82% of patients. The study identified one clinical TLS case and six laboratory TLS cases. Significant TLS factors included BL histology, elevated baseline LDH (⟩500 U/l), and rasburicase usage. Infusion reactions were rare (3%). Median progression‐free survival was 2.6 years, and 2‐year overall survival was 33%, irrespective of TLS occurrence.

Conclusion:

In this real‐life study, clinical TLS occurrence was low (1%). TLS appeared more frequent in BL but did not impact overall survival. Fractionated initial rituximab dosing in addition to preventive strategies is a feasible approach in preventing clinical TLS, warranting further prospective investigation.

News (Medical) associated with Rasburicase

25 Oct 2024

·www.prnewswire.com

Protalix BioTherapeutics to Present Phase I PRX-115 Data in Late-Breaking Poster at ACR Convergence 2024

CARMIEL, Israel, Oct. 25, 2024 /PRNewswire/ -- Protalix BioTherapeutics, Inc. (NYSE American:PLX), a biopharmaceutical company focused on the development, production and commercialization of recombinant therapeutic proteins produced by its proprietary ProCellEx® plant cell–based protein expression system, today announced that data from the phase I clinical trial of PRX-115, the Company's recombinant PEGylated uricase product candidate in development for the treatment of uncontrolled gout, will be presented in a late-breaking poster at the American College of Rheumatology (ACR) Convergence 2024, being held November 14-19, 2024 at the Walter E. Washington Convention Center in Washington, D.C. Details of the presentation are as follows: ACR Convergence 2024 Title: Prolonged Plasma Urate-Lowering After a Single Intravenous Administration of PRX-115, a Novel PEGylated Uricase, in Participants with Elevated Urate Levels Session: Late-Breaking Posters (L01-L14) Session Date/Time: Monday, November 18, 2024, 10:30 AM – 12:30 PM Eastern Standard Time Presenting Author: Orit Cohen Barak, Ph.D. (Protalix Ltd.) Abstract Number: L05 The accepted abstract can be accessed on the ACR Convergence 2024 website at . A copy of the poster will be made available on the Protalix website. About Protalix BioTherapeutics, Inc. Protalix is a biopharmaceutical company focused on the development and commercialization of recombinant therapeutic proteins expressed through its proprietary plant cell-based expression system, ProCellEx. It is the first company to gain U.S. Food and Drug Administration (FDA) approval of a protein produced through plant cell-based in suspension expression system. This unique expression system represents a new method for developing recombinant proteins in an industrial-scale manner. Protalix has licensed to Pfizer Inc. the worldwide development and commercialization rights to taliglucerase alfa for the treatment of Gaucher disease, Protalix's first product manufactured through ProCellEx, excluding in Brazil, where Protalix retains full rights. Protalix's second product, Elfabrio®, was approved by both the FDA and the European Medicines Agency in May 2023. Protalix has partnered with Chiesi Farmaceutici S.p.A. for the global development and commercialization of Elfabrio. Protalix's development pipeline consists of proprietary versions of recombinant therapeutic proteins that target established pharmaceutical markets, including the following product candidates: PRX–115, a plant cell-expressed recombinant PEGylated uricase for the treatment of uncontrolled gout; PRX–119, a plant cell-expressed long action DNase I for the treatment of NETs–related diseases; and others. Forward-Looking Statements To the extent that statements in this press release are not strictly historical, all such statements are forward-looking, and are made pursuant to the safe-harbor provisions of the Private Securities Litigation Reform Act of 1995. The terms "expect," "anticipate," "believe," "estimate," "project," "may," "plan," "will," "would," "should" and "intend," and other words or phrases of similar import are intended to identify forward-looking statements. These forward-looking statements are subject to known and unknown risks and uncertainties that may cause actual future experience and results to differ materially from the statements made. These statements are based on our current beliefs and expectations as to such future outcomes. Drug discovery and development involve a high degree of risk and the final results of a clinical trial may be different than the preliminary findings for the clinical trial. Factors that might cause material differences include, among others: failure or delay in the commencement or completion of clinical trials which may be caused by several factors, including: slower than expected rates of patient recruitment; unforeseen safety issues; determination of dosing issues; lack of effectiveness during clinical trials; inability to satisfactorily demonstrate non-inferiority to approved therapies; inability or unwillingness of medical investigators and institutional review boards to follow our clinical protocols; inability to monitor patients adequately during or after treatment; and/or lack of sufficient funding to finance our clinical trials; the risk that our product candidates will not have the desired effects or will be associated with undesirable side effects or other unexpected characteristics; our dependence on performance by third-party providers of services and supplies, including without limitation, clinical trial services; the inherent risks and uncertainties in developing drug platforms and products of the type we are developing; the impact of development of competing therapies and/or technologies by other companies; potential product liability risks, and risks of securing adequate levels of related insurance coverage; the possible disruption of our operations due to terrorist activities and armed conflict, including as a result of the disruption of the operations of certain regulatory authorities and of certain of our suppliers, collaborative partners, licensees, clinical trial sites, distributors and customers; and other factors described in our filings with the U.S. Securities and Exchange Commission. The statements in this press release are valid only as of the date hereof and we disclaim any obligation to update this information, except as may be required by law. Investor Contact Mike Moyer, Managing Director LifeSci Advisors +1-617-308-4306 [email protected] Logo - SOURCE Protalix BioTherapeutics, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Phase 1Drug ApprovalClinical Result

24 Oct 2024

·www.globenewswire.com

XORTX Sponsored Study Presented at the American Society of Nephrology – Kidney Week 2024

● Health consequences of chronically high uric acid and xanthine oxidase in polycystic kidney disease in rats, mice and humans ● CALGARY, Alberta, Oct. 24, 2024 (GLOBE NEWSWIRE) -- XORTX Therapeutics Inc. ("XORTX" or the “Company”) (NASDAQ: XRTX | TSXV: XRTX | Frankfurt: ANU), a late-stage clinical pharmaceutical company focused on developing innovative therapies to treat progressive kidney disease, is pleased to announce the acceptance of an abstract submitted to the American Society of Nephrology (the “ASN”). The abstract entitled "Xanthine oxidase in rats, mice and humans with polycystic kidney disease" was reviewed by the ASN review panel for scientific merit and novel discoveries. The study was conducted at the University of Colorado in the independent laboratory of Dr. Charles Edelstein and was sponsored by XORTX and will be presented during the Session Title: Genetic Diseases: Cystic - Therapeutic Investigations and Prognosis. Selected results from the study include: In both Rat or Mouse models of Polycystic Kidney Disease (“PKD”) i) Use of a uricase inhibitor to increase uric acid resulted in increased cyst growthii) Xanthine oxidase (“XO”) inhibitor – Oxypurinol – decreased serum uric acid and cyst growthiii) Increased XO staining in kidney and liver was abundant Prospective / Retrospective Clinical Results of the Halt Clinical Trial - Group A - Early PKD patients iv) Patients with increased serum uric acid had increased total kidney volumev) Patients with increased serum uric acid had faster PKD progressionvi) Increase serum XO activity was associated with an earlier onset of high blood pressure About this Study The XO enzyme is an essential enzyme within the uric acid pathway, and is required for the breakdown of purine nucleotides. Uric acid as well as reactive oxygen species released during the enzymatic reaction may also play a detrimental role in the circulatory system and within tissue during disease. Recent pioneering discoveries in rodent models of PKD implicate over expression or over activity of XO. It is currently unknown if XO over expression or over activity in humans is associated with PKD or more rapid progression of disease. The aim of the study was to gain insight into whether increased XO activity results in cyst growth, XO activity was measured in PCK1 rats, PKD1RC/RC (RC) mice and 34 patients from the HALT-PKD Clinical study. The abstract outlines study results from rat, mice and human studies of PKD. The purpose of the study was to gain and understanding of serum xanthine oxidase activity (XOa) in PKD during varied stages of disease and further to relate that activity to total kidney volume, and decline of glomerular filtration rate (GFR). The results of the study provide understanding of where aberrant purine metabolism in PKD tissue due to sources XO enzyme may contribute to circulating uric acid levels, expansion rate of kidney and cyst and functional GFR decline. Prior study results suggested over expression of XO in PKD kidney tissue may be a feature of cystic disease. Dr. Allen Davidoff, CEO of XORTX commented, “Exploring and understanding the contribution of chronically increased serum uric acid and/or the effect of too much or too active XO enzyme in the circulation or tissue on PKD disease progression was a goal of this study. The study results presented today are another pioneering first step towards characterizing how and when to treat individuals with PKD as well as how they might benefit from the Company’s XRx-008 program, and our upcoming registration clinical trial. This study was a preliminary investigation of individuals with early stage PKD, and provided information regarding the health consequences of hyperuricemia and XO. The Company will continue to add to this exciting discovery with future exploration of later stage PKD, assessment of genetic factors contributing to aberrant purine metabolism, including XO overexpression, and this precision medicine opportunity.” About XORTX Therapeutics Inc. XORTX is a pharmaceutical company with two clinically advanced products in development: 1) our lead, XRx-008 program for ADPKD; and 2) our secondary program in XRx-101 for acute kidney and other acute organ injury associated with Coronavirus / COVID-19 infection. In addition, XRx-225 is a pre-clinical stage program for Type 2 Diabetic Nephropathy. XORTX is working to advance its clinical development stage products that target aberrant purine metabolism and xanthine oxidase to decrease or inhibit production of uric acid. At XORTX, we are dedicated to developing medications to improve the quality of life and health of kidney disease patients. Additional information on XORTX is available at www.xortx.com. For more information, please contact: Allen Davidoff, CEONick Rigopulos, Director of Communicationsadavidoff@xortx.com or +1 403 455 7727nick@alpineequityadv.com or +1 617 901 0785 Neither the TSX Venture Exchange nor Nasdaq has approved or disapproved the contents of this news release. No stock exchange, securities commission or other regulatory authority has approved or disapproved the information contained herein. Forward Looking Statements This press release contains express or implied forward-looking statements pursuant to applicable securities laws. These forward-looking statements include, but are not limited to, the Company's beliefs, plans, goals, objectives, expectations, assumptions, estimates, intentions, future performance, other statements that are not historical facts and statements identified by words such as "expects", "anticipates", "intends", "plans", "believes", "seeks", "estimates" or words of similar meaning. These forward-looking statements and their implications are based on the current expectations of the management of XORTX only, and are subject to a number of factors and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Such risks, uncertainties, and other factors include, but are not limited to, our ability to obtain additional financing; the accuracy of our estimates regarding expenses, future revenues and capital requirements; the success and timing of our preclinical studies and clinical trials; the performance of third-party manufacturers and contract research organizations; our plans to develop and commercialize our product candidates; our plans to advance research in other kidney disease applications; and, our ability to obtain and maintain intellectual property protection for our product candidates. Except as otherwise required by applicable law and stock exchange rules, XORTX undertakes no obligation to publicly release any revisions to these forward-looking statements to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events. More detailed information about the risks and uncertainties affecting XORTX is contained under the heading “Risk Factors” in XORTX’s Annual Report on Form 20-F filed with the SEC, which is available on the SEC's website, www.sec.gov (including any documents forming a part thereof or incorporated by reference therein), as well as in our reports, public disclosure documents and other filings with the securities commissions and other regulatory bodies in Canada, which are available on www.sedarplus.ca.

Clinical ResultClinical Study

24 Oct 2024

·www.xortx.com

XORTX Sponsored Study Presented at the American Society of Nephrology – Kidney Week 2024

● Health consequences of chronically high uric acid and xanthine oxidase in polycystic kidney disease in rats, mice and humans ● CALGARY, Alberta, Oct. 24, 2024 (GLOBE NEWSWIRE) -- XORTX Therapeutics Inc. ("XORTX" or the “Company”) (NASDAQ: XRTX | TSXV: XRTX | Frankfurt: ANU), a late-stage clinical pharmaceutical company focused on developing innovative therapies to treat progressive kidney disease, is pleased to announce the acceptance of an abstract submitted to the American Society of Nephrology (the “ASN”). The abstract entitled "Xanthine oxidase in rats, mice and humans with polycystic kidney disease" was reviewed by the ASN review panel for scientific merit and novel discoveries. The study was conducted at the University of Colorado in the independent laboratory of Dr. Charles Edelstein and was sponsored by XORTX and will be presented during the Session Title: Genetic Diseases: Cystic - Therapeutic Investigations and Prognosis. Selected results from the study include: In both Rat or Mouse models of Polycystic Kidney Disease (“PKD”) i) Use of a uricase inhibitor to increase uric acid resulted in increased cyst growth ii) Xanthine oxidase (“XO”) inhibitor – Oxypurinol – decreased serum uric acid and cyst growth iii) Increased XO staining in kidney and liver was abundant Prospective / Retrospective Clinical Results of the Halt Clinical Trial - Group A - Early PKD patients iv) Patients with increased serum uric acid had increased total kidney volume v) Patients with increased serum uric acid had faster PKD progression vi) Increase serum XO activity was associated with an earlier onset of high blood pressure About this Study The XO enzyme is an essential enzyme within the uric acid pathway, and is required for the breakdown of purine nucleotides. Uric acid as well as reactive oxygen species released during the enzymatic reaction may also play a detrimental role in the circulatory system and within tissue during disease. Recent pioneering discoveries in rodent models of PKD implicate over expression or over activity of XO. It is currently unknown if XO over expression or over activity in humans is associated with PKD or more rapid progression of disease. The aim of the study was to gain insight into whether increased XO activity results in cyst growth, XO activity was measured in PCK1 rats, PKD1RC/RC (RC) mice and 34 patients from the HALT-PKD Clinical study. The abstract outlines study results from rat, mice and human studies of PKD. The purpose of the study was to gain and understanding of serum xanthine oxidase activity (XOa) in PKD during varied stages of disease and further to relate that activity to total kidney volume, and decline of glomerular filtration rate (GFR). The results of the study provide understanding of where aberrant purine metabolism in PKD tissue due to sources XO enzyme may contribute to circulating uric acid levels, expansion rate of kidney and cyst and functional GFR decline. Prior study results suggested over expression of XO in PKD kidney tissue may be a feature of cystic disease. Dr. Allen Davidoff, CEO of XORTX commented, “Exploring and understanding the contribution of chronically increased serum uric acid and/or the effect of too much or too active XO enzyme in the circulation or tissue on PKD disease progression was a goal of this study. The study results presented today are another pioneering first step towards characterizing how and when to treat individuals with PKD as well as how they might benefit from the Company’s XRx-008 program, and our upcoming registration clinical trial. This study was a preliminary investigation of individuals with early stage PKD, and provided information regarding the health consequences of hyperuricemia and XO. The Company will continue to add to this exciting discovery with future exploration of later stage PKD, assessment of genetic factors contributing to aberrant purine metabolism, including XO overexpression, and this precision medicine opportunity.” About XORTX Therapeutics Inc. XORTX is a pharmaceutical company with two clinically advanced products in development: 1) our lead, XRx-008 program for ADPKD; and 2) our secondary program in XRx-101 for acute kidney and other acute organ injury associated with Coronavirus / COVID-19 infection. In addition, XRx-225 is a pre-clinical stage program for Type 2 Diabetic Nephropathy. XORTX is working to advance its clinical development stage products that target aberrant purine metabolism and xanthine oxidase to decrease or inhibit production of uric acid. At XORTX, we are dedicated to developing medications to improve the quality of life and health of kidney disease patients. Additional information on XORTX is available at www.xortx.com. Neither the TSX Venture Exchange nor Nasdaq has approved or disapproved the contents of this news release. No stock exchange, securities commission or other regulatory authority has approved or disapproved the information contained herein. Forward Looking Statements This press release contains express or implied forward-looking statements pursuant to applicable securities laws. These forward-looking statements include, but are not limited to, the Company's beliefs, plans, goals, objectives, expectations, assumptions, estimates, intentions, future performance, other statements that are not historical facts and statements identified by words such as "expects", "anticipates", "intends", "plans", "believes", "seeks", "estimates" or words of similar meaning. These forward-looking statements and their implications are based on the current expectations of the management of XORTX only, and are subject to a number of factors and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Such risks, uncertainties, and other factors include, but are not limited to, our ability to obtain additional financing; the accuracy of our estimates regarding expenses, future revenues and capital requirements; the success and timing of our preclinical studies and clinical trials; the performance of third-party manufacturers and contract research organizations; our plans to develop and commercialize our product candidates; our plans to advance research in other kidney disease applications; and, our ability to obtain and maintain intellectual property protection for our product candidates. Except as otherwise required by applicable law and stock exchange rules, XORTX undertakes no obligation to publicly release any revisions to these forward-looking statements to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events. More detailed information about the risks and uncertainties affecting XORTX is contained under the heading “Risk Factors” in XORTX’s Annual Report on Form 20-F filed with the SEC, which is available on the SEC's website, www.sec.gov (including any documents forming a part thereof or incorporated by reference therein), as well as in our reports, public disclosure documents and other filings with the securities commissions and other regulatory bodies in Canada, which are available on www.sedarplus.ca. Released October 24, 2024

Clinical ResultClinical Study

100 Deals associated with Rasburicase

External Link

KEGG	Wiki	ATC	Drug Bank
D05704	Rasburicase	V03AF07	DB00049

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Hyperuricemia	EU	Sanofi Winthrop Industrie SA	23 Feb 2001
Hyperuricemia	IS	Sanofi Winthrop Industrie SA	23 Feb 2001
Hyperuricemia	LI	Sanofi Winthrop Industrie SA	23 Feb 2001
Hyperuricemia	NO	Sanofi Winthrop Industrie SA	23 Feb 2001

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Hematologic Neoplasms	Phase 3	CN	Sanofi	01 Oct 2007
Leukemia	Phase 3	US	Sanofi	01 Apr 2004
Lymphoma	Phase 3	US	Sanofi	01 Apr 2004
Solid tumor	Phase 3	US	Sanofi	01 Apr 2004
Tumor Lysis Syndrome	Phase 3	US	Sanofi	01 Apr 2004
Neoplasms	Phase 2	US	Sanofi	01 Jan 2008
Aggressive Non-Hodgkin Lymphoma	Phase 2	BE	Sanofi	01 Jul 2002
Aggressive Non-Hodgkin Lymphoma	Phase 2	FR	Sanofi	01 Jul 2002
Aggressive Non-Hodgkin Lymphoma	Phase 2	DE	Sanofi	01 Jul 2002
Aggressive Non-Hodgkin Lymphoma	Phase 2	IT	Sanofi	01 Jul 2002

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESMO2023	Not Applicable	Neoplasms	715	Rasburicase	hbhhthwzmu(knjntdxnjr) = mmykgycxqk bgantyjlqk (ykscdfhpzt ) View more	-	23 Oct 2023
ESMO2023	Not Applicable	Neoplasms	715	Allopurinol	hbhhthwzmu(knjntdxnjr) = ljioapagik bgantyjlqk (ykscdfhpzt ) View more	-	23 Oct 2023
ERA2023	Not Applicable	Cardio-Renal Syndrome	23	Rasburicase	xeyihzsixm(nmneethjrv) = jdkqxgtvsm grkdqlwxvw (xfgarmcleg ) View more	-	15 Jun 2023
EULAR2022	Not Applicable	Arthritis, Gouty	17	Rasburicase 1.5mg/d	srcfaovwhl(qfwsdsqlrn) = djhvovlzwz ooccukwnnq (zfoxchgjeu ) View more	-	01 Jun 2022
EHA2020	Not Applicable	Tumor Lysis Syndrome \| Leukemia \| Lymphoma	55	Low dose Rasburicase	aupmxywahc(ykwmulixuz) = mfjlbrpsqn bzfpckwucd (likffkgcei )	Positive	14 May 2020
NCT01200485 (CTgov)	Phase 2	Tumor Lysis Syndrome \| Leukemia \| Lymphoma	55	Rasburicase (Arm A (Rasburicase))	plusbtjixz(hwtvnmpbeg) = hnmjhxenwq ipcomertlh (jgzxfbnkeo, ytqympkkfa - nrauzbxpdl) View more	-	31 Jan 2020
NCT01200485 (CTgov)	Phase 2	Tumor Lysis Syndrome \| Leukemia \| Lymphoma	55	Allopurinol (Arm B (Allopurinol))	plusbtjixz(hwtvnmpbeg) = vzldliipue ipcomertlh (jgzxfbnkeo, zsqficcdov - gwlzlywyvs) View more	-	31 Jan 2020
EHA2019	Not Applicable	Hematologic Neoplasms	-	Low dose rasburicase	tmwnezivkk(aicrxnqxtx) = lhhfewkcga cnjvpyqudd (hjegtnxqpg ) View more	-	16 May 2019
NCT00513474 (CTgov)	Phase 1	Myelodysplastic-Myeloproliferative Diseases \| Multiple Myeloma \| Myeloproliferative Disorders ... View more	46	allogeneic hematopoietic stem cell transplantation+cyclosporin-A+Etoposide+rasburicase+Fludarabine+Busulfan+cyclophosphamide+Tacrolimus+sirolimus+methotrexate (Rasburicase Group)	kfpoomjiaf(zadhftmopb) = osxehwgqvq aqdakgjcxq (nthxuvyshu, okbqfffyki - hhukfdgmnf) View more	-	11 Apr 2017
NCT00513474 (CTgov)	Phase 1		46	allogeneic hematopoietic stem cell transplantation+cyclosporin-A+Etoposide+Fludarabine+Busulfan+cyclophosphamide+Tacrolimus+sirolimus+allopurinol+methotrexate (Control Group)	kfpoomjiaf(zadhftmopb) = dkhtevfcbl aqdakgjcxq (nthxuvyshu, lpmvorglyo - bldnhkmilo) View more	-	11 Apr 2017
ASN2015	Not Applicable	Rhabdomyolysis CPK \| serum myoglobin	-	Rasburicase	nnmjdokjoc(xinhlmqrlz) = cmgvhewwhd btwlisyndg (nztjyeljgu )	Positive	03 Nov 2015
ASN2015	Not Applicable	Urate nephropathy	-	Rasburicase	uqeqsyxfng(nftzioslvo) = jbmcjaoaka znelrxbvln (abntfrbojy ) View more	Positive	03 Nov 2015
ASN2014	Not Applicable	Urate nephropathy Serum uric acid	-	Rasburicase	mntnccqiuh(bzdgjjifvx) = icrqriqyre ftzchfidiq (udbmahrpvr )	Positive	11 Nov 2014

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