Filanesib TFA
Based on 7 publication(s) in Google Scholar
Filanesib TFA (ARRY-520 TFA) is a selective and noncompetitive kinesin spindle protein (KSP) inhibitor, with an IC50 of 6 nM for human KSP. Filanesib TFA induces cell death by apoptosis in vitro. Filanesib TFA has potent anti-proliferative activity.
For research use only. We do not sell to patients.
- CAS No.: 1781834-99-8
- Formula: C22H23F5N4O4S
- Molecular Weight:534.50
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
-
HY-50759
IspinesibKSP Inhibitor -
HY-12069
SB-743921 hydrochlorideEg5 Inhibitor -
HY-15187
FilanesibKSP Inhibitor -
HY-14846
LitronesibKinesin Inhibitor -
HY-19966
K858 (Racemic)Apoptosis Inducer -
HY-12241
AZ82KIFC1 Inhibitor -
HY-19944
DimethylenastronKinesin Inhibitor -
HY-15000
EMD534085Kinesin Inhibitor -
HY-15857
CW-069HSET Inhibitor -
HY-16062
ARQ 621Eg5 Inhibitor -
HY-110208
BRD9876 -
HY-112915
Eg5 Inhibitor V, trans-24Kinesin Inhibitor
Publications Citing Use of MedChemExpress (MCE) Filanesib TFA
More
Customer Validation & Images
-
Cell Proliferation/Viability Assay
-
Cell Proliferation/Viability Assay
-
Flow Cytometry
-
Apoptosis Analysis
-
In Vivo Efficacy Study
All Kinesin Isoforms
More
Biological Activity
Description
IC50 & Target
IC50: 6 nM (KSP)[1]
In Vitro
Filanesib TFA induces mitotic arrest in multiple cell lines[1].
Filanesib TFA exhibits anti-proliferative against a broad range of human and rodent tumor cell lines, including a variety of leukemias and solid tumors, with EC50s between 0.4 nM and 14.4 nM[1].
Filanesib (0.001-0.1 nM; 36 hours) TFA induces apoptosis in a dose-dependent manner in HeLa cells[1].
Filanesib (3.13-6.25 nM; 44 hours) TFA causes accumulation of cells in the G2/M phase of the cell cycle in a dose-dependent manner in HeLa cells[1].
Filanesib TFA potently induces cell cycle block and subsequent death in leukemic cells via the mitochondrial pathway and has potential to eradicate AML progenitor cells[2].
Filanesib (3 μM; 6-24 hours) TFA is able to induce caspase-2 activation[3].
Filanesib (0.003-3 μM; 24-48 hours) TFA is cytotoxic in Type II EOC cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS No. 1781834-99-8
-
Molecular Weight 534.50
-
Formula C22H23F5N4O4S
-
SMILES
O=C(N1[C@@](C2=CC=CC=C2)(CCCN)SC(C3=CC(F)=CC=C3F)=N1)N(OC)C.OC(C(F)(F)F)=O
-
Synonyms
ARRY-520 TFA
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (7)
-
Journal Impact Factor
-
Most Recent
-
Cell Discov
Single-cell profiling reveals molecular basis of malignant phenotypes and tumor microenvironments in small bowel adenocarcinomas. [Abstract]2022 Sep 14;8(1):92. PMID: 36104333
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cell Discov. 2022 Sep 14;8(1):92. [Abstract]
Filanesib (0-100 μM; 36 h) inhibited HUTU-80 cell survival in a dose-dependent manner.
-
Cancer Lett
2021 May 28:506:1-10. PMID: 33652084
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2021 May 28:506:1-10. [Abstract]
Filanesib (0-10 nM; 48 h) showed antiproliferative effects in the benign meningioma cell line Ben-Men-1 and the anaplastic cell lines NCH93, IOMM-Lee, and KT21-MG cells.
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2021 May 28:506:1-10. [Abstract]
Filanesib (10 nM; 24, 48, 72 h) induced cell cycle arrest at G2/M-phase in Ben-Men-1, NCH93, IOMM-Lee, and KT21-MG cells.
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2021 May 28:506:1-10. [Abstract]
Filanesib (10 nM; 72 h) induced cell apoptosis in Ben-Men-1, NCH93, IOMM-Lee, and KT21-MG cells.
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2021 May 28:506:1-10. [Abstract]
Filanesib (10 mg/kg; i.p.; once every three days on five occasions) inhibited NCH93 tumor growth in NCH93 tumor-bearing mice.
Filanesib TFA purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2021 May 28:506:1-10. [Abstract]
Filanesib (10 mg/kg; i.p.; once every three days on five occasions) showed a significant reduction of Ki-67-positive cells in tumor sections.
-
NPJ Precis Oncol
Functional screening identifies kinesin spindle protein inhibitor filanesib as a potential treatment option for hepatoblastoma. [Abstract]2025 Apr 25;9(1):122. PMID: 40281281 -
Gene
2025 Jul 5:955:149458. PMID: 40187619 -
-
-
Methods Mol Biol
2018:1711:351-398. PMID: 29344898
Protocols
-
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
-
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
-
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
-
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
-
Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
[2]. BZ Carter, et al. Inhibition of KSP by ARRY-520 Induces Cell Cycle Block and Cell Death via the Mitochondrial Pathway in AML Cells. [Content Brief]
[3]. Ki Hyung Kim, et al. KSP inhibitor ARRY-520 as a substitute for Paclitaxel in Type I ovarian cancer cells. J Transl Med. 2009; 7: 63. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Filanesib TFA Related Classifications
HY-15187B Related Classifications
Powered by Bioz