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 1/2IIT

Open Label Phase 1/2 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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108

Literatures (Medical) associated with Tasquinimod

01 May 2026·CANCER LETTERS

Spatially resolved transcriptomics identifies tumor-stroma-immune networks and therapeutic targets in endocrine-resistant advanced breast cancer treated with Everolimus+Letrozole: insights from the MIRACLE trial

Article

Author: Ying, Jianming ; Ma, Fei ; Fan, Ying ; Tan, Yujing ; Luo, Yang ; Xue, Xuemin ; Wang, Bingzhi ; Chen, Shanshan ; Lan, Bo ; Wang, Jiayu ; Xu, Binghe ; Ji, Danyang ; Xue, Liyan

Breast cancer is the most commonly diagnosed cancer in women globally. Our previous MIRACLE trial (NCT02313051) demonstrated that everolimus plus letrozole (E + L) significantly improves progression-free survival compared with letrozole (L) monotherapy in premenopausal patients with endocrine therapy-resistant, hormone receptor-positive, HER2-non-amplified advanced breast cancer. This study aims to investigate spatially resolved biomarkers linked to survival benefits from E + L to guide precision therapies. Patients from MIRACLE were stratified by overall survival (OS ≤ 3 vs. >3 years). Spatial Whole Transcriptome Atlas analysis was used to evaluate tumor-, immune-, and stroma-specific gene expression, co-expression network patterns, and survival correlations. Among patients with shorter survival (OS ≤ 3 years), we identified a distinctive gene interaction network characterized by tumor-derived S100A9 and CALML5, which is associated with mTORC1 activation. This finding suggests that tasquinimod, an S100A9 inhibitor, could be a viable therapeutic option. Additionally, an interaction between CALML5 and SLPI across tumor and immune areas indicated a potential role in maintaining tumor integrity and mitigating immune-mediated damage. Conversely, patients with longer survival (OS > 3 years) exhibited SERPINA1 as a hub gene linked to estrogen receptor activation, and an interaction between FKBP5 and SESN3 associated with AKT/mTORC1 inhibition within tumor-rich regions. Furthermore, the interaction between MMP11 and COL16A1 in stroma-rich regions suggests that cancer-associated fibroblasts may contribute to improved outcomes. Our study underscores the critical role of spatial gene expression analysis in elucidating the tumor microenvironment and its impact on prognosis in patients undergoing E + L treatment, thereby opening new avenues for targeted interventions.

01 Feb 2026·iScience

Targeted inhibition of M2 macrophages polarization via a PDC attenuates chronic pancreatitis through the PPARα pathway

Article

Author: Kong, Xin ; Guo, Fangyue ; Wu, Yu ; Zhang, Xiaonan ; Zhai, Zhiwen ; Tao, Xufeng ; Xiang, Hong ; Lv, Jing ; Zhao, Xinya ; Dong, Deshi

This study examines the pivotal role of M2-type macrophages in chronic pancreatitis (CP) and the existing challenges in targeted intervention. A peptide-drug conjugate (PDC) was developed for this investigation by linking the S100A9 inhibitor Tasquinimod to a peptide that selectively targets M2 macrophages. In experimental models, this conjugate demonstrated a marked capacity to alleviate pancreatic injury, inflammation, and fibrotic progression. Compared to the free drug, it showed enhanced targeting, greater efficacy, and a reduced toxicity profile without causing significant damage to vital organs. Mechanistic analysis indicated that its effects are mediated through the activation of the peroxisome proliferator-activated receptor α (PPARα) signaling pathway, leading to suppressed phosphorylation of the NF-κB p65 subunit and c-Jun, which in turn inhibits M2 macrophage polarization. These results uncover a functional mechanism and provide a foundation for developing targeted immunomodulatory therapies against CP.

01 Feb 2026·INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

Macrophage-derived S100A9 drives liver fibrosis in Echinococcus multilocularis infection by up-regulating secreted protein acidic and rich in cysteine (SPARC) in hepatic stellate cells

Article

Author: Lü, Guodong ; Zhang, Xue ; Bi, Xiaojuan ; Li, Liang ; Lin, Renyong ; Yang, Ning ; Shi, Bowen ; Zhang, Hongbin ; Xue, Junlong ; Chu, Jin

Alveolar echinococcosis (AE), caused by Echinococcus multilocularis(E. multilocularis) infection, is a severe parasitic disease characterized by progressive liver fibrosis. Although the damage-associated molecular pattern molecule S100A9 has been implicated in some inflammatory and fibrotic diseases, its role in AE induced liver fibrosis remains unclear. This study aimed to elucidate the function and mechanism of S100A9 in E. multilocularis induced liver fibrogenesis. Using proteomic analysis, we identified significant up-regulation of S100A9 in the livers of infected mice. In a stem cell-based fibrosis regression model, S100A9 expression correlated closely with the extent of fibrosis. Cellular localization and macrophage depletion experiments revealed macrophages as the primary source of S100A9. In vitro, recombinant S100A9 directly activated human hepatic stellate cells (HSCs) LX-2, up-regulating fibrotic markers in a time-dependent manner. Proteomic and molecular analyses further identified SPARC as a critical downstream mediator, and SPARC knockdown attenuated S100A9 induced HSCs activation and TGF-β/SMAD signaling. In vivo, pharmacological inhibition of S100A9 with tasquinimod significantly ameliorated liver fibrosis, down-regulated SPARC expression, and suppressed SMAD2/3 phosphorylation. Critically, histopathological analysis of liver tissues from AE patients confirmed that S100A9 expression was predominantly localized to fibrotic areas and positively correlated with fibrosis severity. Collectively, these results demonstrate that macrophage-derived S100A9 promotes HSCs activation and liver fibrosis via SPARC dependent way, mechanism, and its clinical relevance in human AE substantiates the S100A9-SPARC axis as a potential therapeutic target in AE.

28

News (Medical) associated with Tasquinimod

01 Apr 2026

·www.activebiotech.com

Annual Report 2025 Active Biotech AB (publ)

The Annual Report will only be digitally distributed. “Building on progress in 2025, the coming year will focus on the tasquinimod clinical studies in myelofibrosis and intensified business development for laquinimod,” says Active Biotech CEO Helén Tuvesson.

12 Feb 2026

·www.activebiotech.com

Active Biotech Year End Report 2025

FOURTH QUARTER IN BRIEF Active Biotech announced a fully secured rights issue, subject to approval by an extraordinary general meeting, of approximately SEK 70 million before transaction costs (October 17) Active Biotech announced that preclinical data of tasquinimod in combination with T cell activation will be presented at ASH 2025 (November 3) Active Biotech announced that positive preclinical tasquinimod data in myelofibrosis has been published in Blood Advances (November 24). Active Biotech announced that a patent related to a pharmaceutical formulation of tasquinimod will be granted in the United States (November 25). Active Biotech disclosed the outcome of the rights issue (December 10). OTHER SIGNIFICANT EVENTS JAN-DEC 2025 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). Active Biotech reported positive top-line results from the LION study on ocular absorption and distribution of laquinimod in the eye (May 5). Active Biotech reported study results with tasquinimod in heavily pre-treated patients with relapsed refractory multiple myeloma (May 23). EVENTS AFTER THE END OF THE PERIOD Active Biotech receives positive feedback on its clinical study with tasquinimod in myelofibrosis (February 10, 2026) 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 2026-02-12 at 08:30 CEST.

Clinical ResultPhase 2Drug Approval

25 Nov 2025

·www.activebiotech.com

Active Biotech’s patent related to a pharmaceutical formulation of tasquinimod will be granted in the US

“This patent marks an important step in our strategy to optimize the global multi-layer protection for tasquinimod. In addition, tasquinimod is covered by multiple patents and patent applications mainly for medical use in relevant indications and has been granted orphan drug status by the FDA for the treatment of myelofibrosis and multiple myeloma,” said Active Biotech’s CEO Helén Tuvesson. The patent application relates to a pharmaceutical formulation of tasquinimod with a high oral bioavailability.

Orphan Drug

100 Deals associated with Tasquinimod

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KEGG	Wiki	ATC	Drug Bank
-	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
Castration-Resistant Prostatic Cancer	Phase 3	South Korea	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	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Argentina	Apoteket AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Australia	Active Biotech AB	24 Mar 2011
Adenocarcinoma of prostate	Phase 3	Australia	Apoteket 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

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Clinical Result

Indication

Phase

Evaluation

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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	neabbloxfe(iseoejatck) = 0.5 mg qd x1 wk, then 1 mg qd (a single-agent MTD of 1 mg daily after a 1-week dose escalation) maxzuitffa (itnihbggkt ) View more	Positive	26 May 2023
NCT02057666 (TasQ003, CTgov)	Phase 3	Castration-Resistant Prostatic Cancer \| Metastatic castration-resistant prostate cancer	146	Tasquinimod (Tasquinimod)	kzslaktenm(ohjukkhanp) = ltzaeeadxt xtsywlxtwj (xwdhcijztc, nzzozxxyzh - oxgurqcjeq) View more	-	23 Apr 2021
				Placebo (Placebo)	kzslaktenm(ohjukkhanp) = hhplpvzsgj xtsywlxtwj (xwdhcijztc, mopxfpvrfp - qtllvycuai) View more
NCT01743469 (CTgov)	Phase 2	Metastatic Renal Cell Carcinoma \| Ovarian Cancer \| Neoplasm Metastasis ... View more	201	Tasquinimod (Hepatocellular Carcinoma Cohort)	ancnppsvzo = eycycayvwo mbdzhnektf (zmbgauopfa, haijcbykhx - xwgakimafj) View more	-	07 May 2018
				Tasquinimod (Ovarian Carcinoma Cohort)	ancnppsvzo = bpzupfqosm mbdzhnektf (zmbgauopfa, tamqeuktwk - gyibwvtkkf) View more
NCT01732549 (Pubmed \| Ann Oncol) Manual	Phase 2	Metastatic castration-resistant prostate cancer First line	144	tasquinimod	iznlefqexe(uymyjbhohk) = oyxfrtqdxo rcntpvdbac (vcrqfgvldq, 24.3 - 53.7) View more	Positive	01 Nov 2017
				Placebo	iznlefqexe(uymyjbhohk) = fjrhllaxjv rcntpvdbac (vcrqfgvldq, 16.1 - 25.9) View more
NCT01732549 (Pubmed)	Phase 2	Metastatic castration-resistant prostate cancer Maintenance	144	Tasquinimod	kjvchkpfwx(lrecikdwff) = bprnjsycqz ipnayzfafh (zqdzeibmno, 24.3 - 53.7)	Positive	01 Nov 2017
				Placebo	kjvchkpfwx(lrecikdwff) = nzgtsaztns ipnayzfafh (zqdzeibmno, 16.1 - 25.9)
NCT01743469 (Pubmed \| Target Oncol)	Phase 2	Stomach Cancer	201	Tasquinimod (Hepatocellular cancer)	rfwismzdas(eljgmuprqy) = unddznujyo slfvrbvnux (cmnyhcykxn )	Negative	01 Oct 2017
				Tasquinimod (Ovarian cancer)	rfwismzdas(eljgmuprqy) = dayqieycng slfvrbvnux (cmnyhcykxn )
NCT01732549 (CTgov)	Phase 2	Castration-Resistant Prostatic Cancer	144	Tasquinimod (Tasquinimod)	kcbvnvkixq(pmyitkjgns) = cyqexklbqk emsfpeojqu (jqfnukuvoj, rszykdoieq - gxdldrlygx) View more	-	03 Oct 2016
				Placebo (Placebo)	kcbvnvkixq(pmyitkjgns) = wzvmlcgxvr emsfpeojqu (jqfnukuvoj, stxyilnowi - lkbnvxyanl) View more
NCT01234311 (Pubmed \| J Clin Oncol)	Phase 3	Metastatic castration-resistant prostate cancer	-	Tasquinimod	cceypmzoda(txpqcxxfei) = xodnnbdpay azednmkyvs (hstvppecrp, 19.5 - 23.0) View more	Positive	01 Aug 2016
				Placebo	cceypmzoda(txpqcxxfei) = cisypwhomo azednmkyvs (hstvppecrp, 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))	cbcicizjls(qcrmalebza) = lwvpxxzgdl tdjrupbgmy (zxadpquwal, ijhxivjboy - xfpvcvrxcx) View more	-	20 May 2016
				Laboratory Biomarker Analysis+Tasquinimod+Sipuleucel-T (Arm II (Tasquinimod, Sipuleucel-T))	wfyvtddvye = lzlaosnpci bbyzszvhin (lxirsmezbx, gsjcvzvrtg - ilnqumxsic) View more
NCT01732549 (ASCO2013)	Phase 2	Metastatic castration-resistant prostate cancer Maintenance	140	Tasquinimod	aawpwxxofe(bnmlhwdxur) = gjqeadxjjc bemhcexmud (yyvfwgdvxw )	-	20 May 2013
				Placebo	aawpwxxofe(bnmlhwdxur) = pplchfoymc bemhcexmud (yyvfwgdvxw )