Cat. No.: HY-16191

ELR510444

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ELR510444 is an orally active tubulin inhibitor with an IC₅₀ of 10 μM. ELR510444 binds to the colchicine-binding site on β-tubulin, inhibits tubulin assembly, depolymerizes microtubules and blocks HIF activity. ELR510444 induces cellular microtubule loss, abnormal mitotic spindle, mitotic arrest, apoptosis, morphological changes in tumor endothelial cells, and inhibits cancer cell proliferation, angiogenesis and tumor growth. ELR510444 can be used in research related to various cancers such as renal cell carcinoma.

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Pureté: 98.0%
CAS No.: 1233948-35-0
Formule: C₁₉H₁₆N₂O₂S₂
Masse moléculaire:368.47

Stockage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

ELR510444 Chemical Structure

CAS No.: 1233948-35-0

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Activité biologique
- Description
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Publications (1)
Solvant et solubilité
- In Vitro
Pureté et documentation
Références
Help & FAQs
Classifications
Bioz

Activité biologique

Description

Voir tous les produits spécifiques à Isoform HIF/HIF Prolyl-Hydroxylase :

In Vitro

ELR510444 (48 h) potently inhibits the proliferation of various cancer cell lines and endothelial cell lines at low nanomolar concentrations, with relatively low relative resistance in βIII-tubulin-overexpressing HeLa cells (Rr = 1.4) and P-glycoprotein-overexpressing SK-OV-3 cells (Rr = 2.3)^[1].
ELR510444 (18 h) acts as a microtubule depolymerizing agent in rat embryonic aortic smooth muscle cells A-10, with an EC₅₀ of 21 nM for inducing cellular microtubule loss^[1].
ELR510444 (25 nM; 18 h) induces mitotic arrest and formation of compact abnormal multipolar spindles in HeLa cervical cancer cells^[1].
ELR510444 induces apoptosis in HCT-116 cells, with an EC₅₀ of 19 nM for activating caspase 3/7, which is consistent with its antiproliferative mechanism^[1].
ELR510444 (30 nM; 1 h) induces rapid morphological changes (retraction of intercellular junctions, formation of membrane vesicles) in 2H-11 mouse tumor endothelial cells upon treatment at 30 nM for 1 h, suggesting its potential vascular disrupting activity^[1].
ELR510444 (0-100 nM; 16 h) potently inhibits HIF-1α activity in VHL-deficient RCC4 cells, with nearly complete inhibition observed at concentrations ≥ 30 nM^[2].
ELR510444 (0-100 nM; 24 h) reduces the protein expression of HIF-1α and HIF-2α in VHL-deficient RCC4 cells in a dose-dependent manner^[2].
ELR510444 (10 nM; 24 h) significantly reduces the transcriptional level of HIF-1α in VHL-deficient RCC4 cells, as well as the transcriptional level of HIF-2α in VHL-deficient RCC4, 786-O and A498 cells^[2].
ELR510444 (10 nM; 16 h) significantly reduces VEGF secretion in VHL-deficient A498, RCC4 and 786-O renal cell carcinoma cells^[2].
ELR510444 (0-1000 nM; 72 h) reduces cell viability in all tested renal cell carcinoma cell lines, and exerts more significant efficacy in VHL-deficient A498, 786-O and RCC4 cells compared with VHL-proficient ACHN, Caki-1 and Caki-2 cells^[2].
ELR510444 (3-30 nM; 24 h) reduces the clonogenic survival rate of all tested renal cell carcinoma cell lines, and exerts more significant efficacy on VHL-deficient A498, 786-O and RCC4 cells compared with VHL-proficient ACHN, Caki-1 and Caki-2 cells^[2].
ELR510444 (10-30 nM; 24 h) induces apoptosis in all tested renal cell carcinoma cell lines; it exhibits selective activity against VHL-deficient A498, 786-O and RCC4 cells at a concentration of 10 nM, and acts on all cell lines at 30 nM^[2].
Studies show that introduction of VHL into VHL-deficient A498 and 786-O renal cell carcinoma cells significantly reduces the sensitivity of these cells to apoptosis induced by 10 nM ELR510444 (10 nM; 24 h)^[2].
ELR510444 (10 nM; 24 h) reduces the expression level of HIF-2α protein in vector-only-transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells under both basal and hypoxic (CoCl₂-treated) conditions^[2].
ELR510444 (10 nM; 16 h) reduces VEGF secretion levels in vector-only-transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells under both basal and hypoxic (CoCl₂-treated) conditions^[2].
ELR510444 (0-30 nM; 72 h) reduces the viability of vector-only transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells, and its efficacy against VHL-transfected cells is enhanced under hypoxic conditions (treated with CoCl₂)^[2].
ELR510444 (10-30 nM; 24 h) induces mitotic arrest and apoptosis in all tested renal cell carcinoma cell lines at the concentration of 30 nM, while it preferentially induces apoptosis in VHL-deficient cell lines at 10 nM^[2].
ELR510444 (20-35 nM; 24 h) destabilizes microtubules in RCC4 renal cancer cells, with an EC₅₀ of 27 nM, and significant depolymerization is observed at concentrations ≥ 20 nM^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[1]

Cell Line:

HeLa cervical cancer cells
Concentration:

25 nM
Incubation Time:

18 h
Result:

Caused accumulation of HeLa cells with tetraploid DNA content (mitotic arrest) and induced formation of aberrant, compact, multiple mitotic spindles.

Western Blot Analysis^[2]

Cell Line:

VHL-deficient RCC4 renal cell carcinoma cells
Concentration:

0, 3, 10, 30 and 100 nM
Incubation Time:

24 h
Result:

Induced a dose-dependent decrease in both HIF-1α and HIF-2α protein expression, with visible reduction starting at 0.3 nM and near-complete loss at 100 nM.
Maintained consistent β-tubulin levels across all concentrations.

Real Time qPCR^[2]

Cell Line:

VHL-deficient RCC4, 786-O, and A498 renal cell carcinoma cells
Concentration:

10 nM
Incubation Time:

24 h
Result:

Reduced HIF-1α transcript levels in RCC4 cells with a fold change ~-1.2 relative to control.
Reduced HIF-2α transcript levels in 786-O, RCC4, and A498 cell.

ELISA Assay^[2]

Cell Line:

VHL-deficient A498, RCC4, and 786-O renal cell carcinoma cells
Concentration:

10 nM
Incubation Time:

16 h
Result:

Decreased VEGF secretion in all three cell lines: from ~2100 pg/mL to ~1100 pg/mL in A498, ~1500 pg/mL to ~800 pg/mL in RCC4, and ~1300 pg/mL to ~800 pg/mL in 786-O.

Apoptosis Analysis^[2]

Cell Line:

VHL-deficient (A498, 786-O, RCC4) and VHL-proficient (ACHN, Caki-1, Caki-2) renal cell carcinoma cells
Concentration:

10 and 30 nM
Incubation Time:

24 h
Result:

Stimulated apoptosis in all tested RCC cell lines.
Induced 20-45% DNA fragmentation in VHL-deficient lines at 10 nM, compared to 10-20% in VHL-proficient lines.
Induced 25-45% DNA fragmentation in all lines at 30 nM.

Apoptosis Analysis^[2]

Cell Line:

VHL-transfected and vector-only control A498 and 786-O renal cell carcinoma cells
Concentration:

10 nM
Incubation Time:

24 h
Result:

Induced ~20% DNA fragmentation in vector-only A498 cells and ~17% in vector-only 786-O cells, compared to ~8-9% in VHL-transfected A498 and 786-O cells.

Western Blot Analysis^[2]

Cell Line:

VHL-transfected and vector-only control A498 and 786-O renal cell carcinoma cells treated with hypoxia mimic (CoCl₂)
Concentration:

10 nM
Incubation Time:

24 h
Result:

Reduced HIF-2α levels under both basal and hypoxic (CoCl₂-treated) conditions in both vector and VHL-transfected cells, despite CoCl₂ stimulating HIF-2α expression in VHL-transfected cells.

ELISA Assay^[2]

Cell Line:

VHL-transfected and vector-only control A498 and 786-O renal cell carcinoma cells treated with hypoxia mimic (CoCl₂)
Concentration:

10 nM
Incubation Time:

16 h
Result:

Reduced VEGF secretion under both basal and hypoxic (CoCl₂-treated) conditions in both vector and VHL-transfected cells, with levels corresponding to reduced HIF-2α expression.

Cell Cycle Analysis^[2]

Cell Line:

VHL-deficient (A498, 786-O, RCC4) and VHL-proficient (ACHN, Caki-1, Caki-2) renal cell carcinoma cells
Concentration:

10 and 30 nM
Incubation Time:

24 h
Result:

Induced mitotic (G2/M) arrest and increased sub-G0/G1 apoptotic cells in all tested RCC lines at 30 nM.
Induced apoptosis preferentially in VHL-deficient lines without prominent G2/M arrest at 10 nM.

Immunofluorescence^[2]

Cell Line:

RCC4 renal cell carcinoma cells
Concentration:

20, 25, 30 and 35 nM
Incubation Time:

24 h
Result:

Induced microtubule destabilization in a dose-dependent manner, with detectable depolymerization starting at 15 nM, visible effects in most cells at 20 nM, and an EC₅₀ of 27 nM for microtubule loss.

Parmacokinetics

Species	Dose	Route	C_max	T_1/2
Mice^[1]	25 mg/kg	p.o.	1.2 μg/mL	3.6 h

In Vivo

ELR510444 (3-12.5 mg/kg; p.o.; daily; 28 days) exhibits dose-dependent in vivo antitumor efficacy in a MDA-MB-231 breast cancer xenograft model^[1].
ELR510444 (8 mg/kg; p.o.; QDx5; 2 weeks) significantly reduces tumor volume by ~55%, inhibits tumor angiogenesis, increases tumor necrosis, and induces tumor cell and endothelial cell apoptosis in the 786-O RCC xenograft model^[2].
ELR510444 (8 mg/kg; p.o.; QDx5; 2 weeks) significantly reduces tumor volume by ~46%, inhibits tumor angiogenesis, increases tumor necrosis, and induces tumor cell and endothelial cell apoptosis in the A498 RCC xenograft model^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

BALB/c nude (female, 6 to 7 weeks of age)^[1]
Dosage:

3 mg/kg; 6 mg/kg; 12.5 mg/kg
Administration:

p.o.; daily; 28 days
Result:

Caused dose-dependent antitumor effects.
Demonstrated antitumor activity comparable with positive control ABT-751 at 75 mg/kg at 6 mg/kg dose.
Showed no additional antitumor activity at 12.5 mg/kg maximum tolerated dose compared with 6 mg/kg dose.
Maintained animal body weight during first 2 weeks of treatment, with only minor weight loss in last 2 weeks that never dropped below initial body weight.
Achieved at least a 2-fold therapeutic window.

Animal Model:

BALB/c nude mice (female)^[2]
Dosage:

8 mg/kg
Administration:

p.o.; QDx5; 2 weeks
Result:

Decreased mean tumor volume by ~55% compared to vehicle controls.
Reduced PCNA-positive cells to ~35% from ~85% in controls.
Increased cleaved caspase-3 positive cells to ~10% from ~1.5% in controls.
Elevated central tumor necrosis to 60% from 5% in controls.
Reduced mean vessel density to 16 from 39 in controls.
Increased endothelial cell apoptosis to 7% from 1% in controls.
Reduced VEGF relative intensity to ~0.65 from ~1.7 in controls.
Caused no significant animal weight loss.\nDecreased mean tumor volume by ~46% compared to vehicle controls.
Reduced PCNA-positive cells to ~32% from ~90% in controls.
Increased cleaved caspase-3 positive cells to ~12% from ~1% in controls.
Elevated central tumor necrosis to 27% from 4% in controls.
Reduced mean vessel density to 12 from 34 in controls.
Increased endothelial cell apoptosis to 8% from 0.5% in controls.
Reduced VEGF relative intensity to ~0.6 from ~1.55 in controls.
Caused no significant animal weight loss.

Chemical Information

CAS No. 1233948-35-0
Appearance Solid
Masse moléculaire 368.47
Formule C₁₉H₁₆N₂O₂S₂
Color Light yellow to yellow
SMILES

O=S(C1=CC=C(C)C=C1)(NC2=CC(C3=CC=C(C#N)S3)=CC=C2C)=O
Livraison

Room temperature in continental US; may vary elsewhere.

Stockage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (1)

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RSC Adv

Structural insights into targeting of the colchicine binding site by ELR510444 and parbendazole to achieve rational drug design. [Abstract]

2021 May 25;11(31):18938-18944. PMID: 35478655

Solvant et solubilité

In Vitro:

DMSO : ≥ 37 mg/mL (100.42 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.7139 mL

13.5696 mL

27.1392 mL

5 mM

0.5428 mL

2.7139 mL

5.4279 mL

10 mM

0.2714 mL

1.3570 mL

2.7139 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Calculateur de molarité

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Calculateur de dilution

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

Fiche technique (289 KB)
SDS (392 KB)
- English - EN (392 KB)
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- Norwegian - NO (392 KB)
- Español - ES (392 KB)
- Swedish - SV (392 KB)
- Italian - IT (392 KB)
- Korean - KR (392 KB)
- Portuguese - PT (392 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Instruction de manipulation (2659 KB)

Références

[1]. Risinger AL, et al. ELR510444, a novel microtubule disruptor with multiple mechanisms of action. J Pharmacol Exp Ther. 2011;336(3):652-660. [Content Brief]

[2]. Carew JS, et al. ELR510444 inhibits tumor growth and angiogenesis by abrogating HIF activity and disrupting microtubules in renal cell carcinoma. PLoS One. 2012;7(1):e31120. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.7139 mL	13.5696 mL	27.1393 mL	67.8481 mL
	5 mM	0.5428 mL	2.7139 mL	5.4279 mL	13.5696 mL
	10 mM	0.2714 mL	1.3570 mL	2.7139 mL	6.7848 mL
	15 mM	0.1809 mL	0.9046 mL	1.8093 mL	4.5232 mL
	20 mM	0.1357 mL	0.6785 mL	1.3570 mL	3.3924 mL
	25 mM	0.1086 mL	0.5428 mL	1.0856 mL	2.7139 mL
	30 mM	0.0905 mL	0.4523 mL	0.9046 mL	2.2616 mL
	40 mM	0.0678 mL	0.3392 mL	0.6785 mL	1.6962 mL
	50 mM	0.0543 mL	0.2714 mL	0.5428 mL	1.3570 mL
	60 mM	0.0452 mL	0.2262 mL	0.4523 mL	1.1308 mL
	80 mM	0.0339 mL	0.1696 mL	0.3392 mL	0.8481 mL
	100 mM	0.0271 mL	0.1357 mL	0.2714 mL	0.6785 mL

ELR510444

1 Cited Publications

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ELR510444

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Immunology/Inflammation Compound Library

Metabolism/Protease Compound Library

Anti-Cancer Compound Library

Anti-Aging Compound Library

Reprogramming Compound Library

Oxygen Sensing Compound Library

Cytoskeleton Compound Library

Glutamine Metabolism Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Angiogenesis-Related Compound Library

Transcription Factor-Targeted Library

Protein-protein Interaction Inhibitor Library

Cancer Stem Cells Compound Library

Metabolic Enzyme Compound Library

Cell Death Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Bioactive Compound Library

Anti-Fibrosis Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

Lactic Acid Metabolic Compound Library

High-Throughput Bioactive Compound Library

High-Efficiency Gene Editing Compound Library

Publications Citing Use of MedChemExpress (MCE) ELR510444

Voir tous les produits spécifiques à Isoform HIF/HIF Prolyl-Hydroxylase

Activité biologique

Chemical Information

Publications (1)

Solvant et solubilité

Pureté et documentation

Références

Help & FAQs

Complete Stock Solution Preparation Table

ELR510444 Related Classifications

HY-16191 Related Classifications