2. Cell Cycle/DNA Damage Cytoskeleton Apoptosis Metabolic Enzyme/Protease
  3. Microtubule/Tubulin Apoptosis HIF/HIF Prolyl-Hydroxylase Mitosis
  4. ELR510444

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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ELR510444

ELR510444 Chemical Structure

CAS No. : 1233948-35-0

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Based on 1 publication(s) in Google Scholar

ELR510444 Related Antibodies

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1 Publications Citing Use of MCE ELR510444

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Description

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[1][2].

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.

ELR510444 Related Antibodies

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 Cmax T1/2
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.
Molecular Weight

368.47

Formula

C19H16N2O2S2
CAS No.
Appearance

Solid

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
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 2 years
-20°C 1 year
Solvent & Solubility
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.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.7139 mL 13.5696 mL 27.1392 mL
5 mM 0.5428 mL 2.7139 mL 5.4279 mL
View the Complete Stock Solution Preparation Table

* 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.

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Purity & Documentation
References

Complete Stock Solution Preparation Table

* 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.

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
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

ELR5104441233948-35-0ELR 510444ELR-510444Microtubule/TubulinApoptosisHIF/HIF Prolyl-HydroxylaseMitosisHypoxia-inducible factorsHIFsHIF-PHSK-OV-3 cellscolchicine-binding siteHeLa cellsRCC4 cellsHCT-116 cellsβ-tubulinA-10 embryonic rat aortic smooth muscle cellsHIF-1α2H-11 murine tumor endothelial cellsHIF-2αInhibitorinhibitorinhibit

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