Delving into the Latest Updates on Tasquinimod with Synapse

The goal of this clinical trial is to learn if therapy can be improved in patients with myelofibrosis (MF) who have primary resistance or who have progressed after treatment with a Janus kinase (JAK) inhibitor or are intolerant for this category of drugs.
The main questions it aims to answer are:
* To evaluate the feasibility and safety of once daily dose of tasquinimod for 24 weeks (6 cycles)
* To determine the optimal dose
Patients will be treated once daily with tasquinimod for a maximum period of 24 weeks (6 cycles).
During the study most (diagnostic) procedures are part of the standard of care. Different from standard of care:
* Participation may lead to extra visits to the outpatient clinic
* Additional blood will be drawn when blood is already taken per standard of care
* Bone marrow sampling at entry and at the end of the trial
* MRI scans (or CT-scans) have to be performed
* Quality-of-life questionnaires have to be filled out

Start Date20 Feb 2025

Sponsor / Collaborator

Hemato-Oncologie voor Volwassenen Nederland

NCT06327100

/ RecruitingPhase 2IIT

Open Label Phase 2 Study of Tasquinimod in Patients With Primary Myelofibrosis (PMF), Post-Polycythemia Vera Myelofibrosis (Post-PV MF), or Post-Essential Thrombocytosis Myelofibrosis (Post-ET MF)

To learn if tasquinimod either alone or in combination with ruxolitinib can help to control PMF, post-PV MF, or post-ET MF.

Start Date01 Aug 2024

Sponsor / Collaborator

The University of Texas MD Anderson Cancer Center

[+1]

ACTRN12621000016831

/ Not yet recruitingPhase 2

A randomized, double-blind, placebo-controlled phase II trial to evaluate the efficacy of tasquinimod in reducing the time taken for a 2-point decrease in admission status.in adults with COVID-19

Start Date15 Dec 2022

Sponsor / Collaborator

Hunter Medical Research Institute

100 Clinical Results associated with Tasquinimod

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100 Translational Medicine associated with Tasquinimod

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100 Patents (Medical) associated with Tasquinimod

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111

Literatures (Medical) associated with Tasquinimod

01 Mar 2025·CELLULAR SIGNALLING

Aerobic plus resistance exercise attenuates skeletal muscle atrophy induced by dexamethasone through the HDAC4/FoxO3a pathway

Article

Author: Tian, Jiatong ; Wang, Danni ; Ma, Jianxiong ; Liu, Sujuan ; Liang, Dehuan ; Xiang, Heng ; Niu, Yanmei ; Zheng, Xinyue ; Yu, Chunxia

This study aimed to investigate the underlying mechanisms by which physical exercise mitigates muscle atrophy induced by Dexamethasone (Dex). A muscle atrophy model was established in the mouse C2C12 cell line and 8-week-old mice treated with Dex, with subsequent verification of phenotype and atrogene expression. The potential benefits of combined aerobic and resistance exercise in mitigating muscle atrophy were then examined. To elucidate the involvement of Histone deacetylase 4 (HDAC4) in the protective effects of exercise against muscle loss, a combination of RT-PCR, Western blotting, immunoprecipitation, and immunofluorescence staining techniques were employed. The upregulation of HDAC4 was observed following Dex-induced muscle atrophy in vitro and in vivo. Inhibition of HDAC4 in C2C12 cells resulted in an increase in myotube diameter and fusion index, along with a decrease in the expression of Atrogin-1 and MuRF1. Treatment with Tasquinimod, an HDAC4 inhibitor, effectively prevented muscle wasting and dysfunction in mice induced by Dex. After a 6-week exercise intervention, the Dex-Exercise group exhibited significant improvements in body fat level, hyperinsulinemia, muscle mass and function in comparison to the Dex-Sedentary group. Mechanistically, we discovered that HDAC4 bound to and deacetylated Forkhead box protein O 3a (FoxO3a) within the nucleus, leading to decreased phosphorylation of FoxO3a at Ser 253. This interaction subsequently facilitated the expression of downstream atrogene Atrogin-1 and MuRF1, resulting in muscle atrophy. Conversely, exercise was found to potentially mitigate muscle atrophy by inhibiting the HDAC4/FoxO3a pathway. These findings suggest that HDAC4 may be a potential therapeutic target for exercise to combat Dex-induced muscle atrophy.

01 Mar 2025·KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY

Tasquinimod promotes the sensitivity of ovarian cancer cells to cisplatin by down-regulating the HDAC4/p21 pathway

Article

Author: Min, Xiao-Jia ; Lin, Ying ; Wu, Ya-Hong ; Li, Zhao ; Guo, Ye-Qing

To investigate whether Tasquinimod can influence cisplatin resistance in drug-resistant ovarian cancer (OC) cell lines by regulating histone deacetylase 4 (HDAC4) or p21, we explored its effects on the cell cycle, and associated mechanisms. RT-PCR and Western blot analyses, flow cytometry, CCK8 assay, and immunofluorescence were utilized to investigate the effects of Tasquinimod on gene expression, cell cycle, apoptosis, viability, and protein levels in OC cells. The results showed that Tasquinimod inhibited cell viability and promoted apoptosis in SKOV3/DDP (cisplatin) and A2780/DDP cells more effectively than DDP alone. In combination with cisplatin, Tasquinimod further enhanced cell apoptosis and reduced cell viability in these cell lines, an effect that could be reversed following HDAC4 overexpression. Tasquinimod treatment down-regulated HDAC4, Bcl-2, and cyclin D1, and CDK4 expression and up-regulated the cleaved-Caspase-3, and p21 expression in SKOV3/DDP and A2780/ DDP cells. Additionally, Tasquinimod inhibited DDP resistance in OC/DDP cells. These effects were similarly observed in OC mouse models treated with Tasquinimod. In conclusion, Tasquinimod can improve OC cells' sensitivity to DDP by down-regulating the HDAC4/p21 axis, offering insights into potential strategies for overcoming cisplatin resistance in OC.

01 Jun 2024·Bioactive materials

Enhanced osteochondral regeneration with a 3D-Printed biomimetic scaffold featuring a calcified interfacial layer

Article

Author: Yu, Mingzhao ; Zhang, Changqing ; Yin, Wenjing ; Wu, Di ; Hu, Bin ; Deng, Jue ; Yu, Qingxiao ; Zheng, Kaiwen ; Wei, Xiaojuan

The integrative regeneration of both articular cartilage and subchondral bone remains an unmet clinical need due to the difficulties of mimicking spatial complexity in native osteochondral tissues for artificial implants. Layer-by-layer fabrication strategies, such as 3D printing, have emerged as a promising technology replicating the stratified zonal architecture and varying microstructures and mechanical properties. However, the dynamic and circulating physiological environments, such as mass transportation or cell migration, usually distort the pre-confined biological properties in the layered implants, leading to undistinguished spatial variations and subsequently inefficient regenerations. This study introduced a biomimetic calcified interfacial layer into the scaffold as a compact barrier between a cartilage layer and a subchondral bone layer to facilitate osteogenic-chondrogenic repair. The calcified interfacial layer consisting of compact polycaprolactone (PCL), nano-hydroxyapatite, and tasquinimod (TA) can physically and biologically separate the cartilage layer (TA-mixed, chondrocytes-load gelatin methacrylate) from the subchondral bond layer (porous PCL). This introduction preserved the as-designed independent biological environment in each layer for both cartilage and bone regeneration, successfully inhibiting vascular invasion into the cartilage layer and preventing hyaluronic cartilage calcification owing to devascularization of TA. The improved integrative regeneration of cartilage and subchondral bone was validated through gross examination, micro-computed tomography (micro-CT), and histological and immunohistochemical analyses based on an in vivo rat model. Moreover, gene and protein expression studies identified a key role of Caveolin (CAV-1) in promoting angiogenesis through the Wnt/β-catenin pathway and indicated that TA in the calcified layer blocked angiogenesis by inhibiting CAV-1.

20

News (Medical) associated with Tasquinimod

23 May 2025

·www.activebiotech.com

Active Biotech reports study results with tasquinimod in heavily pre-treated patients with relapsed refractory multiple myeloma

“These results confirm the feasibility of combining tasquinimod in an all-oral combination with standard-of-care agents for patients with multiple myeloma who have exhausted other treatment options,” said Dr. Dan Vogl, Principal Investigator. In this analysis, a total of 17 patients received tasquinimod in combination with IRd. During dose-escalation, no dose-limiting toxicities were observed, and dose level two (tasquinimod 1 mg daily after a one week run-in at 0.5 mg daily) was selected as the dose for the expansion cohort. Patients were heavily pretreated with a median of 7 prior lines of therapy (range 4-19) and all were triple-class refractory with 71% (12 pts) refractory to their most recent Imid/PI combination. Among these 12 patients, there was one durable Partial Response (PR) and three Minimal Responses (MR). These data are in line with previously reported results confirming the safety, tolerability and anti-myeloma effect of tasquinimod alone and in combination with IRd in patients with relapsed refractory multiple myeloma. ”Importantly, the observed responses in patients with myeloma previously refractory to an Imid/PI combination, who would not be expected to respond to the IRd backbone regimen, suggest synergistic efficacy of tasquinimod with IRd. These results highlight the potential for targeting the tumor microenvironment as a way to augment the efficacy of other myeloma therapies,” said Dr. Vogl. The study (NCT04405167), which is conducted at Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, has closed to enrolment, and the full study results are being analyzed. The abstract is available online on https://meetings.asco.org/ after 5 PM (ET) on May 22. Details on the presentation: Abstract Title: Clinical Activity of Novel Targeting of S100A9 with Tasquinimod for Relapsed and Refractory Multiple Myeloma (RRMM) Session Title: Hematologic Malignancies – Plasma Cell Dyscrasia Abstract Number: 7555 Session Date and Time: June 1, 2025, 8:00 AM-12:00 AM (ET)

Clinical ResultClinical Study

21 May 2025

·www.activebiotech.com

Active Biotech announces patent for tasquinimod in myelofibrosis granted in Europe

“We are very pleased that this significant patent has been granted by the EPO. It is an important step in the development program for tasquinimod in hematological malignancies, with a primary focus on myelofibrosis,” said Active Biotech’s CEO Helén Tuvesson. The patent, with the European patent number, 4185292 provides protection and market exclusivity in strategic European markets through 2041 for the use of tasquinimod in treatment of myeloproliferative neoplasms (MPN) i.e. myelofibrosis. The patent, issued in the name of Erasmus University Medical Center (Erasmus MC), Rotterdam was licensed exclusively to Active Biotech from Oncode Institute, acting on behalf of Erasmus MC, in 2022.

Patent Expiration

08 May 2025

·www.activebiotech.com

Active Biotech Interim Report Q1 2025

FIRST QUARTER IN BRIEF US Patent Office granted Active Biotech’s patent application for laquinimod in eye disorders (January 28) Active Biotech announced that the first patient was enrolled in the European clinical study of tasquinimod in myelofibrosis (February 24) Active Biotech announced that the first patient was dosed in the phase II study of tasquinimod in myelofibrosis in the US (March 10) EVENTS AFTER THE END OF THE PERIOD Active Biotech reported positive top-line results from the LION study on ocular absorption and distribution of laquinimod in the eye (May 5) FINANCIAL SUMMARY The report is also available at www.activebiotech.com The information was submitted, through the agency of the contact person below, for public disclosure on 2025-05-08 at 08:30 CEST. Active Biotech AB (Corp. reg. no. 556223-9227) / Scheelevägen 22, SE-223 63 Lund / +46 46 19 20 00

Clinical ResultPhase 2Financial Statement

100 Deals associated with Tasquinimod

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-	Tasquinimod	-	DB05861

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Castration-Resistant Prostatic Cancer	Phase 3	China	Ipsen SA	01 Jan 2014
Adenocarcinoma of prostate	Phase 3	United States	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	United States	Apoteket AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Argentina	Apoteket AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Argentina	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Australia	Apoteket AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Australia	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Belgium	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Belgium	Apoteket AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Brazil	Apoteket AB	24 Mar 2011

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Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04405167 (ASCO 12023 \| ASCO 22023) Manual	Phase 1	Relapse multiple myeloma	10	tasquinimod	xzigpeqxho(lrewxfjimj) = 0.5 mg qd x1 wk, then 1 mg qd (a single-agent MTD of 1 mg daily after a 1-week dose escalation) rbzbvmukxu (qpihcfkzdk ) View more	Positive	26 May 2023
NCT02057666 (TasQ003, CTgov)	Phase 3	Castration-Resistant Prostatic Cancer \| Metastatic castration-resistant prostate cancer	146	Tasquinimod (Tasquinimod)	lnqpncwthl(vrhdrnfmli) = soelttfkev dgbbywtile (yywvhxymhd, jpoxcpqymu - mmkwazzgns) View more	-	23 Apr 2021
				Placebo (Placebo)	lnqpncwthl(vrhdrnfmli) = exyqazkwwq dgbbywtile (yywvhxymhd, vvajoudgza - edapnztezc) View more
NCT01743469 (CTgov)	Phase 2	Metastatic Renal Cell Carcinoma \| Ovarian Cancer \| Neoplasm Metastasis ... View more	201	Tasquinimod (Hepatocellular Carcinoma Cohort)	aqahaumtnp = vcglwusvmk isyupdtdsd (lbhhelpbnm, kxhmrvnnyc - hwzeniieoq) View more	-	07 May 2018
				Tasquinimod (Ovarian Carcinoma Cohort)	aqahaumtnp = vmgpuddwcy isyupdtdsd (lbhhelpbnm, fpqiufyxcg - elebozybks) View more
NCT01732549 (Pubmed \| Ann Oncol) Manual	Phase 2	Metastatic castration-resistant prostate cancer First line	144	tasquinimod	hpqsqcawae(qlyetwsdnw) = pzwhspbyit yegplwlldb (zexrrqzmpz, 24.3 - 53.7) View more	Positive	01 Nov 2017
				Placebo	hpqsqcawae(qlyetwsdnw) = kuntslznrp yegplwlldb (zexrrqzmpz, 16.1 - 25.9) View more
NCT01732549 (Pubmed)	Phase 2	Metastatic castration-resistant prostate cancer Maintenance	144	Tasquinimod	pkgeswmkkt(vjhghswcoq) = qmjrjkdxhj wzxeqkmkhp (tzmzyponuf, 24.3 - 53.7)	Positive	01 Nov 2017
				Placebo	pkgeswmkkt(vjhghswcoq) = rubhhuvczz wzxeqkmkhp (tzmzyponuf, 16.1 - 25.9)
NCT01743469 (Pubmed \| Target Oncol)	Phase 2	Stomach Cancer	201	Tasquinimod (Hepatocellular cancer)	afpllaxlaz(swduiyckkh) = xnepzdlluz epnxtkpdvj (xispuddosz )	Negative	01 Oct 2017
				Tasquinimod (Ovarian cancer)	afpllaxlaz(swduiyckkh) = rtvfgtoxrl epnxtkpdvj (xispuddosz )
NCT01732549 (CTgov)	Phase 2	Castration-Resistant Prostatic Cancer	144	Tasquinimod (Tasquinimod)	crpnzkbbhc(ulebuxzrgc) = lparybvggu ccpwnjycwv (htpkcbloob, xzqxzmzmhz - bjmcvcotcl) View more	-	03 Oct 2016
				Placebo (Placebo)	crpnzkbbhc(ulebuxzrgc) = jsrtupcmvh ccpwnjycwv (htpkcbloob, cikgilqyhy - jqdzezgerx) View more
NCT01234311 (Pubmed \| J Clin Oncol)	Phase 3	Metastatic castration-resistant prostate cancer	-	Tasquinimod	zzkjxfrfqi(ndkorhyuec) = lqoymwuehv orymzbpirt (amfrvhkawa, 19.5 - 23.0) View more	Positive	01 Aug 2016
				Placebo	zzkjxfrfqi(ndkorhyuec) = lrhtnaktvg orymzbpirt (amfrvhkawa, 21.4 - 26.9) View more
NCT02159950 (CTgov)	Phase 2	Recurrent Prostate Carcinoma \| Castration-Resistant Prostatic Cancer \| Metastatic castration-resistant prostate cancer ... View more	2	Laboratory Biomarker Analysis+Sipuleucel-T (Arm I (Sipuleucel-T))	amkrmgoaxg(ezrnqwruxo) = qpokoghndn alqojkwosp (yryvsikjiz, pobxcltbov - oaplpdltjt) View more	-	20 May 2016
				Laboratory Biomarker Analysis+Tasquinimod+Sipuleucel-T (Arm II (Tasquinimod, Sipuleucel-T))	shyzzjtlwb = ggasnvbswq aeewbuaucm (wvyuzuzacl, nqepefmwiv - ifvnmqifha) View more
NCT01732549 (ASCO2013)	Phase 2	Metastatic castration-resistant prostate cancer Maintenance	140	Tasquinimod	infxrjvfqo(gmhhubqfkc) = guxyztljwk cyxwzlpiyk (cumcxiutdc )	-	20 May 2013
				Placebo	infxrjvfqo(gmhhubqfkc) = vkotfscwbo cyxwzlpiyk (cumcxiutdc )