Biological Activity

Bioactivity / Mechanism

Erastin inhibits system x_c− function in cell-based transport assays. Glutamate-release IC50 values were 0.20 µM in HT-1080 cells and 0.14 µM in Calu-1 cells; these values describe transport inhibition rather than direct binding or cell killing. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
Ferroptosis

Cellular Effect

Cell Line	Activity	Value	Description	Reference
BJ	IC50	0.9 μM	Induction of cell death in human BJ cells expressing TERT, LT, ST and RAS G12V mutant genes cells in presence of PD-98059 by trypan blue exclusion method	[PMID: 17568748]
BJ	IC50	0.9 μM	Induction of cell death in human BJ cells expressing TERT, LT, ST and RAS G12V mutant genes cells in presence of MEK inhibitor 2 by trypan blue exclusion method	[PMID: 17568748]
BJ	IC50	2 μM	Induction of cell death in human BJ cells expressing TERT, LT, ST and RAS G12V mutant genes cells in presence of MEK 1/2 inhibitor by trypan blue exclusion method	[PMID: 17568748]
BJ	IC50	2.6 μM	Induction of cell death in human BJ cells expressing TERT, LT, ST and RAS G12V mutant genes in presence of MEK inhibitor by trypan blue exclusion method	[PMID: 17568748]
BJ	IC50	31.2 μM	Induction of cell death in human BJ cells expressing TERT, LT, ST and RAS G12V mutant genes in presence of U0126 by trypan blue exclusion method	[PMID: 17568748]
Calu-1	IC50	4 μM	Inhibition of human Calu1 cells expressing KRAS with activating mutations by trypan blue exclusion assay	[PMID: 17568748]
CCF-STTG1	IC50	200 nM	Inhibition of Xct in human CCF-STTG1 cells assessed as glutamate release after 2 hrs by fluorometry	[PMID: 26231156]
HT-1080	IC50	1 μM	Induction of cell death in human HT1080 cells in presence of PD-98059 by trypan blue exclusion method	[PMID: 17568748]
HT-1080	IC50	1.3 μM	Induction of cell death in human HT1080 cells in presence of MEK inhibitor 2 by trypan blue exclusion method	[PMID: 17568748]
HT-1080	IC50	2.5 μM	Induction of cell death in human HT1080 cells in presence of MEK inhibitor by trypan blue exclusion method	[PMID: 17568748]
HT-1080	IC50	3.4 μM	Induction of cell death in human HT1080 cells in presence of U0126 by trypan blue exclusion method	[PMID: 17568748]
HT-1080	IC50	6 μM	Induction of cell death in human HT1080 cells in presence of MEK 1/2 inhibitor by trypan blue exclusion method	[PMID: 17568748]

12 records · Scroll to view more

In Vitro Studies

Erastin reduced clonogenic survival in HeLa and NCI-H1975 cells after 24 h exposure. Ferrostatin-1 partly rescued survival, with weaker rescue in NCI-H1975 cells, indicating model-dependent contributions to the cytotoxic response. [2]

Cell-based inhibition of system xc− function

Cell-based study · HT-1080 human fibrosarcoma and Calu-1 human lung carcinoma cells [1]

Erastin inhibited glutamate release in a cell-based transport assay. Inactive erastin-A8 and SLC7A11 silencing provided mechanistic controls. Total glutamate release included other transporters, so maximal inhibition was incomplete.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Inhibition of glutamate release in HT-1080 cells	IC50 0.20 µM (95% C.I. 0.11–0.34 µM)	[1]
Inhibition of glutamate release in Calu-1 cells	IC50 0.14 µM (95% C.I. 0.081–0.21 µM)	[1]

Literature-Reported Treatment Conditions

Exposure duration: 1 h compound exposure
Method: Amplex Red enzyme-coupled measurement of glutamate released into Na+-containing, glutamine-free medium; normalized to cell number and DMSO controls.
Vehicle: DMSO control
Reported limits: Dose range for Figure 2H and final DMSO percentage not specified in selected method text.

Methods and source locations

Compound reported in the paper: Erastin; Compound label in the paper: Parent erastin

Applies to parent erastin in the reported model; no salt, stereoisomer, analog or Adooq lot equivalence is established.

Figure 2C–H; Results: Erastin inhibits system xc− function potently and specifically; Methods: Chemicals; Medium-throughput glutamate release assay

Inhibition of glutamate release in HT-1080 cells: Cell-based transport-function readout, not binding affinity or cytotoxicity; Figure 2 data from three independent biological replicates, plotted mean ± SD. — Figure 2H and accompanying Results; medium-throughput assay method

Inhibition of glutamate release in Calu-1 cells: Same cell-based glutamate-release assay; three independent biological replicates, plotted mean ± SD. — Figure 2H and accompanying Results; medium-throughput assay method

Erastin cytotoxicity and ferrostatin-1 rescue

Cell-based study · HeLa cervical and NCI-H1975 lung adenocarcinoma cells [2]

Erastin reduced clonogenic survival in both cell lines. Ferrostatin-1 partly suppressed this effect, with weaker rescue in NCI-H1975 than in HeLa cells.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Clonogenic survival after erastin ± ferrostatin-1	Treatment comparison Dose-dependent survival loss; ferrostatin-1 partly rescued survival (p < 0.0001 for ferrostatin-1 treatment in both lines).	[2]

Literature-Reported Treatment Conditions

Treatment concentration: Erastin: 0.1, 1, 5, 10, 20 or 50 µM
Exposure duration: 24 h exposure, followed by compound removal and 9 days colony growth
Method: Clonogenic assay; colonies with more than 50 cells counted as surviving.
Co-treatment: With or without 1 µM ferrostatin-1; this study record does not include irradiation.
Reported limits: Cell-treatment solvent and its final percentage not specified in the retrieved cell-treatment method; animal vehicle is not transferred here.

Methods and source locations

Compound reported in the paper: Erastin; Compound label in the paper: Parent erastin

Applies to parent erastin in the reported model; no salt, stereoisomer, analog or Adooq lot equivalence is established.

Figure 1 image/caption; Results: Erastin induces ferroptosis in the human adenocarcinoma cell lines; Discussion paragraph 1; Reagents; drug treatment and clonogenic assay methods

Clonogenic survival after erastin ± ferrostatin-1: Mean ± S.E., n = 3 as reported; two-way ANOVA. n is not further redefined here. — Figure 1 and caption; associated Results and Discussion

In Vivo Studies

In NCI-H1975 xenografts, erastin combined with local X-ray irradiation reduced tumor growth versus control. Erastin alone did not significantly suppress growth under the tested regimen; the combination result should not be read as single-agent efficacy. [2]

Short-course erastin treatment in healthy mice lowered hemoglobin and red-cell counts. Platelet count and serum ALT/AST did not change significantly in that experiment. The findings support a model- and regimen-specific tolerability limitation. [3]

Tumor-growth response to erastin with local irradiation

Animal study · NCI-H1975 subcutaneous xenografts in female BALB/c Slc-nu/nu mice, 8–10 weeks old [2]

The combination group had lower tumor growth than control. Erastin alone and radiation alone did not significantly suppress tumor growth under this regimen.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Tumor volume 14 days after irradiation	Mean ± S.E. Control 1753.84 ± 288.67; X-ray 1738.52 ± 309.95; erastin 1719.07 ± 203.13; combination 1079.89 ± 227.84 mm³.	[2]

Conditions shared by the study groups

Vehicle: 5% DMSO/corn oil for erastin; exact control injection schedule not separately detailed.

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Control	—	Day 14: 1753.84 ± 288.67 mm³; n = 5.	[2]
X-ray alone 3 Gy	Control	Day 14: 1738.52 ± 309.95 mm³; n = 5; no significant growth suppression.	[2]
Erastin alone 15 mg/kg/day	Control	Day 14: 1719.07 ± 203.13 mm³; n = 5; no significant growth suppression.	[2]
Erastin + X-ray Erastin 15 mg/kg/day; X-ray 3 Gy	Control and single-treatment groups	Day 14: 1079.89 ± 227.84 mm³; n = 6; lower tumor growth than control (p < 0.05, repeated-measures two-way ANOVA).	[2]

Control: Model: NCI-H1975 subcutaneous xenografts in female BALB/c Slc-nu/nu mice, 8–10 weeks old; Reported limits: Blinding and a prospective power calculation not described in the selected animal methods.

X-ray alone: Model: NCI-H1975 subcutaneous xenografts in female BALB/c Slc-nu/nu mice, 8–10 weeks old; Route: Local X-ray irradiation; Frequency: Single irradiation; Treatment course: One irradiation; Reported limits: Blinding and a prospective power calculation not described in the selected animal methods.

Erastin alone: Model: NCI-H1975 subcutaneous xenografts in female BALB/c Slc-nu/nu mice, 8–10 weeks old; Route: Intraperitoneal; Frequency: Every 24 h; Treatment course: 3 days; Reported limits: Blinding and a prospective power calculation not described in the selected animal methods.

Erastin + X-ray: Model: NCI-H1975 subcutaneous xenografts in female BALB/c Slc-nu/nu mice, 8–10 weeks old; Route: Intraperitoneal erastin; local X-ray irradiation; Frequency: Erastin every 24 h; one irradiation; Treatment course: Erastin for 3 days; irradiation 24 h after last injection; Reported limits: Blinding and a prospective power calculation not described in the selected animal methods.

Methods and source locations

Compound reported in the paper: Erastin; Compound label in the paper: Parent erastin

Applies to parent erastin in the reported model; no salt, stereoisomer, analog or Adooq lot equivalence is established.

Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

Tumor volume 14 days after irradiation: n = 5 per control/single-treatment group; n = 6 combination. Repeated-measures two-way ANOVA; Figure 4A marks combination vs control p < 0.05. — Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

Control · Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

X-ray alone · Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

Erastin alone · Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

Erastin + X-ray · Figure 4A and caption; Results: Treatment with erastin potentiates radiotherapy and decreases glutathione concentration in tumor xenograft models; animal model, administration and statistical methods

Short-course erastin alters blood indices in healthy mice

Animal study · Healthy male C57BL/6 mice, 8 weeks old, 20–21 g; erastin n = 6, solvent control n = 6 [3]

The erastin group had lower hemoglobin, hematocrit, red-cell count and red-cell distribution width. Platelet count and serum ALT/AST did not differ significantly. These data limit claims of tumor-selective tolerability.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Blood hemoglobin; control versus erastin	Mean ± SEM 164.30 ± 2.73 versus 155.50 ± 1.56 g/l; p = 0.04	[3]
Red blood cell count; control versus erastin	Mean ± SEM 10.43 ± 0.15 versus 9.76 ± 0.13 × 10¹²/l; p = 0.01	[3]
Platelet count, ALT and AST; control versus erastin	Mean ± SEM Platelets: 959.70 ± 56.82 versus 830.50 ± 75.40 × 10⁹/l (p = 0.20); ALT: 37.40 ± 2.58 versus 33.80 ± 3.54 U/l (p = 0.44); AST: 135.00 ± 9.26 versus 158.00 ± 13.94 U/l (p = 0.19).	[3]

Conditions shared by the study groups

Route: Intraperitoneal
Vehicle: 5% DMSO + 40% PEG400 + 5% Tween-80 + 50% physiological saline

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Solvent control	—	Reference blood indices in Table I.	[3]
Erastin 25 mg/kg body weight	Solvent-treated mice, n = 6	Lower hemoglobin, hematocrit, red-cell count and red-cell distribution width; platelet count and ALT/AST were not significantly different.	[3]

Solvent control: Model: Healthy male C57BL/6 mice, 8 weeks old, 20–21 g; erastin n = 6, solvent control n = 6; Frequency: Control schedule not separately restated; Treatment course: 2-day comparison; Reported limits: Randomization, blinding and a rescue arm establishing ferroptosis-specific causality for hematological changes not described in the reported two-group design.

Erastin: Model: Healthy male C57BL/6 mice, 8 weeks old, 20–21 g; erastin n = 6, solvent control n = 6; Frequency: At 12-h intervals; Treatment course: 2 days; sampling 6 h after last injection; Reported limits: Randomization, blinding and a rescue arm establishing ferroptosis-specific causality for hematological changes not described in the reported two-group design.

Methods and source locations

Compound reported in the paper: Erastin; Compound label in the paper: Parent erastin

Applies to parent erastin in the reported model; no salt, stereoisomer, analog or Adooq lot equivalence is established.

Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Blood hemoglobin; control versus erastin: n = 6 mice/group in Animals; statistical section specifies mean ± SEM and unpaired two-tailed Student’s t-test. — Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Red blood cell count; control versus erastin: Same hematology design and statistical reporting. — Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Platelet count, ALT and AST; control versus erastin: Same two-group design; these null tests do not establish equivalence or general safety. — Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Solvent control · Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Erastin · Table I (publisher PDF page 3); Methods: Animals; Statistical analysis; Results first subsection

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	571203-78-6
Applications	VDAC inhibitor
Formula	C₃₀H₃₁ClN₄O₄
Molecular Weight	547.04
SMILES	CCOC1=CC=CC=C1N2C(=O)C3=CC=CC=C3N=C2C(C)N4CCN(CC4)C(=O)COC5=CC=C(C=C5)Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	17 mg/mL (31.07 mM)
Water	Insoluble
Ethanol	Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration: 1.66 mg/mL
Vehicle: 5%DMSO+40%PEG 300+5%Tween80+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Scott J Dixon, Darpan N Patel, Matthew Welsch, et al. Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis eLife (2014). PMID: 24844246 DOI: 10.7554/eLife.02523 Source material
[2] Yuki Shibata, Hironobu Yasui, Kei Higashikawa, et al. Erastin, a ferroptosis-inducing agent, sensitized cancer cells to X-ray irradiation via glutathione starvation in vitro and in vivo PLoS ONE (2019). PMID: 31800616 DOI: 10.1371/journal.pone.0225931 Source material
[3] Jing Zhao, Ben Xu, Qingqing Xiong, et al. Erastin-induced ferroptosis causes physiological and pathological changes in healthy tissues of mice Molecular Medicine Reports (2021). PMID: 34396451 DOI: 10.3892/mmr.2021.12352 Source material

Publications

8 publications citing this product

Mao Yang, .et al. , Biochem Biophys Res Commun, 2025, Sep 5:784:152599 PMID: 40972362
Xuejie Huan, .et al. , Neurosci Bull, 2024, Dec 12 PMID: 39666195
Filiz Bakar-Ates, .et al. , Naunyn Schmiedebergs Arch Pharmacol, 2024, Oct 11 PMID: 39392483
Filiz Bakar-Ates, .et al. , Toxicol In Vitro, 2024, Feb:94:105732 PMID: 37956772
Sureya Nijiati, .et al. , Mol Pharm, 2023, Oct 2;20(10):5185-5194 PMID: 37711135
Erva Ozkan, .et al. , Life Sci, 2023, Jan 1;312:121222 PMID: 36442526
Yuki Shibata, .et al. , Biochem Biophys Rep, 2021, Feb 24;26 PMID: 33681481
Shibata Y, .et al. , PLoS One, 2019, Dec 4;14(12):e0225931 PMID: 31800616

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Erastin

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Biological Activity

Bioactivity / Mechanism

Target & Activity

Cellular Effect

In Vitro Studies

Cell-based inhibition of system xc− function

Literature-Reported Treatment Conditions

Erastin cytotoxicity and ferrostatin-1 rescue

Literature-Reported Treatment Conditions

In Vivo Studies

Tumor-growth response to erastin with local irradiation

Conditions shared by the study groups

Short-course erastin alters blood indices in healthy mice

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

In Vivo Preparation

Storage

Research References

Publications

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