Tasquinimod

Antiangiogenic and antineoplastic agent CAS# 254964-60-8

Tasquinimod

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Chemical structure

Tasquinimod

3D structure

Chemical Properties of Tasquinimod

Cas No. 254964-60-8 SDF Download SDF
PubChem ID 54682876 Appearance Powder
Formula C20H17F3N2O4 M.Wt 406.36
Type of Compound N/A Storage Desiccate at -20°C
Synonyms ABR-215050
Solubility DMSO : ≥ 42 mg/mL (103.36 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[4-(trifluoromethyl)phenyl]quinoline-3-carboxamide
SMILES CN1C2=C(C(=CC=C2)OC)C(=C(C1=O)C(=O)N(C)C3=CC=C(C=C3)C(F)(F)F)O
Standard InChIKey ONDYALNGTUAJDX-UHFFFAOYSA-N
Standard InChI InChI=1S/C20H17F3N2O4/c1-24(12-9-7-11(8-10-12)20(21,22)23)18(27)16-17(26)15-13(25(2)19(16)28)5-4-6-14(15)29-3/h4-10,26H,1-3H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Tasquinimod

DescriptionTasquinimod is an oral antitumor drug.
Targetstumor microenvironment    

Protocol

Cell experiment [1]:

Cell lines

LNCaP cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reacting condition

24 h; 50 μM

Applications

Generated microarray data based on four separate biological replicates showed a drug-induced effect of 50μM tasquinimod on gene expression in LNCaP cells when cultured in vitro for 24 h. The expression data achieved by RT-PCR were consistent with the microarray analysis data with a significant up-regulation of THBS1, GDF15 and CYP1A1 whereas CXCR4 and AGER1 did not change expression significantly.

Animal experiment [2]:

Animal models

Male athymic Nude BALB/c mice (age 8 weeks)

Dosage form

10 mg/kg /day; oral taken

Application

To investigate whether an early treatment could inhibit tumor establishment in addition to the previously shown effects on tumor growth, treatment was initiated directly at subcutaneous inoculation of LNCaP cells and compared to treatment starting 1 week after inoculation, when tumor growth already was established. In the control group the take rate was 100%. By direct treatment the tumor take rate was decreased to 12.5 % by tasquinimod (10 mg/kg/day) compared to 87.5% in the group treated from 1 week after inoculation (P<0.01). In addition, tasquinimod decreased the size of established tumors when treated from day 7.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Olsson A, Björk A, Vallon-Christersson J, et al. Research Tasquinimod (ABR-215050), a quinoline-3-carboxamide anti-angiogenic agent, modulates the expression of thrombospondin-1 in human prostate tumors[J]. 2010.

[2] Jennbacken K, Welen K, Olsson A, et al. Inhibition of metastasis in a castration resistant prostate cancer model by the quinoline‐3‐carboxamide tasquinimod (ABR‐215050)[J]. The Prostate, 2012, 72(8): 913-924.

Tasquinimod Dilution Calculator

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Tasquinimod Molarity Calculator

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Preparing Stock Solutions of Tasquinimod

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.4609 mL 12.3044 mL 24.6087 mL 49.2174 mL 61.5218 mL
5 mM 0.4922 mL 2.4609 mL 4.9217 mL 9.8435 mL 12.3044 mL
10 mM 0.2461 mL 1.2304 mL 2.4609 mL 4.9217 mL 6.1522 mL
50 mM 0.0492 mL 0.2461 mL 0.4922 mL 0.9843 mL 1.2304 mL
100 mM 0.0246 mL 0.123 mL 0.2461 mL 0.4922 mL 0.6152 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Tasquinimod

Tasquinimod is an orally administered quinoline-3-carboxamide with potent antiangiogenic and antitumorigenic ability that has shown promise in the treatment of advanced prostate cancers [1].
Treatment with tasquinimod leads to a remarkable up-regulation in the expression of TSP-1 and down-regulation of VEGF and HIF-1α. The antiangiogenic activities of tasquinimod are therefore due to the dual inhibition of S100A9/TLR4 in MDSCs and the inhibition of HDAC4/N-CoR/HDACs deacetylation of HIF1-α in both endothelial and tumor cells, inhibiting hypoxia induced angiogenesis.
Human endothelial and prostate cancer cells in culture and human prostate cancer xenografts growing in castrated male nude mice were evaluated for their response to radiation alone and in combination with tasquinimod. Due to its potent reduction of the hypoxic response in endothelial cells, cancer cells, TAMs and MDSCs, tasquinimod inhibits tumor angiogenesis while sparing already formed vasculature. The data obtained in vivo and in vitro highlights a potent anticancer effect as a monotherapy in addition to greatly improving the response to combination therapies with docetaxel, androgen deprivation therapy or radiotherapy [1, 3].
At clinically relevant drug levels, tasquinimod significantly enhances anti-cancer efficacy of fractionated radiation with optimal timing for initiating daily tasquinimod treatment being after completion of the fractionated radiation. Phase I and II studies of tasquinimod have demonstrated tasquinimod to be well-tolerated and lead to significant improvements in progression-free survival from metastasis, by a period of 4.3 months, in patients with minimally symptomatic CRPC. The result highlights tasquinimod as an extremely promising and much needed therapeutic tool for use in CRPC [1, 2].
References:
[1]. Williamson SC, Hartley AE, Heer R. A review of tasquinimod in the treatment of advanced prostate cancer. Drug Design Development And Therapy, 2013, 7: 167-174.
[2]. Olsson A, Bjork A, Vallon-Christersson J, et al. Tasquinimod (ABR-215050), a quinoline-3-carboxamide anti-angiogenic agent, modulates the expression of thrombospondin-1 in human prostate tumors. Molecular Cancer, 2010, 9: 107.
[3]. Dalrymple SL, Becker RE, Zhou HM, et al. Tasquinimod prevents the angiogenic rebound induced by fractionated radiation resulting in an enhanced therapeutic response of prostate cancer xenografts. Prostate, 2012, 72(6): 638-648.

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References on Tasquinimod

Tasquinimod modulates tumor-infiltrating myeloid cells and improves the antitumor immune response to PD-L1 blockade in bladder cancer.[Pubmed:27471612]

Oncoimmunology. 2016 Feb 18;5(6):e1145333.

The infiltration of myeloid cells helps tumors to overcome immune surveillance and imparts resistance to cancer immunotherapy. Thus, strategies to modulate the effects of these immune cells may offer a potential therapeutic benefit. We report here that Tasquinimod, a novel immunotherapy which targets S100A9 signaling, reduces the immunosuppressive properties of myeloid cells in preclinical models of bladder cancer (BCa). As single anticancer agent, Tasquinimod treatment was effective in preventing early stage tumor growth, but did not achieve a clear antitumor effect in advanced tumors. Investigations of this response revealed that Tasquinimod induces an increase in the expression of a negative regulator of T cell activation, Programmed-death-ligand 1 (PD-L1). This markedly weakens its antitumor immunity, yet provokes an "inflamed" milieu rendering tumors more prone to T cell-mediated immune attack by PD-L1 blockade. Interestingly, the combination of Tasquinimod with an Anti-PD-L1 antibody enhanced the antitumor immune response in bladder tumors. This combination synergistically modulated tumor-infiltrating myeloid cells, thereby strongly affecting proliferation and activation of effector T cells. Together, our data provide insight into the rational combination of therapies that activate both innate and adaptive immune system, such as the association of S100A9-targeting agents with immune checkpoints inhibitors, to improve the response to cancer immunotherapeutic agents in BCa.

The anti-tumor effect of the quinoline-3-carboxamide tasquinimod: blockade of recruitment of CD11b(+) Ly6C(hi) cells to tumor tissue reduces tumor growth.[Pubmed:27400708]

BMC Cancer. 2016 Jul 11;16:440.

BACKGROUND: Previous work has demonstrated immunomodulatory, anti-tumor, anti-metastatic and anti-angiogenic effects of the small molecule quinoline-3-carboxamide Tasquinimod in pre-clinical cancer models. To better understand the anti-tumor effects of Tasquinimod in transplantable tumor models, we have evaluated the impact of the compound both on recruitment of myeloid cells to tumor tissue and on tumor-induced myeloid cell expansion as these cells are known to promote tumor development. METHODS: Mice bearing subcutaneous 4 T1 mammary carcinoma tumors were treated with Tasquinimod in the drinking water. A BrdU-based flow cytometry assay was utilized to assess the impact of short-term Tasquinimod treatment on myeloid cell recruitment to tumors. Additionally, long-term treatment was performed to study the anti-tumor effect of Tasquinimod as well as its effects on splenic myeloid cells and their progenitors. Myeloid cell populations were also immune-depleted by in vivo antibody treatment. RESULTS: Short-term Tasquinimod treatment did not influence the proliferation of splenic Ly6C(hi) and Ly6G(hi) cells, but instead reduced the influx of Ly6C(hi) cells to the tumor. Treatment with Tasquinimod for various periods of time after tumor inoculation revealed that the anti-tumor effect of this compound mainly operated during the first few days of tumor growth. Similar to Tasquinimod treatment, antibody-mediated depletion of Ly6C(hi) cells within that same time frame, caused reduced tumor growth, thereby confirming a significant role for these cells in tumor development. Additionally, long-term Tasquinimod treatment reduced the splenomegaly and expansion of splenic myeloid cells during a later phase of tumor development. In this phase, Tasquinimod normalized the tumor-induced alterations in myeloerythroid progenitor cells in the spleen but had only limited impact on the same populations in the bone marrow. CONCLUSIONS: Our results indicate that Tasquinimod treatment reduces tumor growth by operating early after tumor inoculation and that this effect is at least partially caused by reduced recruitment of Ly6C(hi) cells to tumor tissue. Long-term treatment also reduces the number of splenic myeloid cells and myeloerythroid progenitors, but these effects did not influence established rapidly growing tumors.

Phase Ib Trial of Cabazitaxel and Tasquinimod in Men With Heavily Pretreated Metastatic Castration Resistant Prostate Cancer (mCRPC): The CATCH Trial.[Pubmed:27862097]

Prostate. 2017 Mar;77(4):385-395.

BACKGROUND: Tasquinimod is an immunomodulating and anti-antiangiogenic oral agent with anti-prostate cancer activity in preclinical studies and in clinical trials of men with metastatic castration resistant prostate cancer (mCRPC), including single agent activity and in combination with taxanes. We sought to identify the maximum tolerated dose (MTD) and recommended phase 2 dose (RP2D) of Tasquinimod in combination with cabazitaxel and prednisone in men with chemorefractory mCRPC. METHODS: Men with mCRPC who had failed prior docetaxel chemotherapy received cabazitaxel 25 mg/m(2) every 3 weeks with oral Tasquinimod at 1 of 3 escalating dose levels (0.25, 0.5, and 1.0 mg once daily) with prednisone and PEG-filgastrim support, using a 3 + 3 dose escalation design. Treatment continued until progressive disease or unacceptable toxicity. RESULTS: We enrolled 25 men with chemorefractory mCRPC. The RP2D was 0.5 mg Tasquinimod based on excess DLTs (two of three men) observed at dose level 3 (1.0 mg) including grade 3 sensory neuropathy and grade 3 atrial fibrillation. Dose level 2 was expanded to 14 men, where 3 DLTs were observed: grade 3 fatigue, grade 4 febrile neutropenia, and grade 3 liver function abnormalities. The proportion of men with a >/=30% PSA decline was 63% and the median composite progression-free survival (PFS) was 8.5 months (95% CI 4.2-16.4 months) based on 12 PFS events. The median number of cycles of cabazitaxel was 6 (range 1-13), with six men receiving >10 cycles. Best overall RECIST responses (CR + PR) were observed in three men (12%), with stable disease in 12 (48%). No pharmacokinetic interactions were observed. CONCLUSIONS: We determined the RP2D of Tasquinimod combined with cabazitaxel to be 0.5 mg daily following a 3 week lead-in of Tasquinimod 0.25 mg with growth factor support. No unexpected toxicities occurred. Prostate 77: 385-395, 2017. (c) 2016 Wiley Periodicals, Inc.

Description

Tasquinimod is an oral antiangiogenic agent, which has the potential for castration-resistant prostate cancer treatment. Tasquinimod binds to the regulatory Zn2+ binding domain of HDAC4 with Kd of 10-30 nM. Tasquinimod also is a S100A9 inhibitor.

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