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Art. -Nr.: HY-181986

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ERX-208

ERX-208 is an anticancer agent that induces endoplasmic reticulum stress by targeting lysosomal acid lipase A (LIPA), ultimately leading to cancer cell apoptosis. ERX-208 can be used in ovarian cancer research.

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CAS. Nr.: 2440087-57-8
Formel: C₄₇H₅₂N₆O₁₀
Molecular Weight:860.95

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

ERX-208 Chemical Structure

CAS. Nr.: 2440087-57-8

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Biologische Aktivität
- Beschreibung
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

In Vitro

ERX-208 (6 days) potently reduces cell viability across all five subtypes of ovarian cancer cells with an IC₅₀ of ~100 nM and shows minimal cytotoxicity toward normal ovarian surface epithelial cells^[1].
ERX-208 significantly impairs the long-term proliferative potential of ovarian cancer cells as measured by colony formation assays^[1].
ERX-208 (500 nM) induces caspase-dependent apoptosis in ovarian cancer cells, with no evidence of ferroptosis or necroptosis induction^[1].
ERX-208 (1 μM; 0-48 h) robustly activates the endoplasmic reticulum stress response in diverse ovarian cancer models at the transcriptional, post-transcriptional, and ultrastructural levels^[1].
ERX-208 (1 μM; 0-16 h) -mediated endoplasmic reticulum stress response and cytotoxicity in SKOV3 ovarian cancer cells are dependent on LIPA expression^[1].
ERX-208 (22 h) potently suppresses the invasive capacity of ascites-derived ovarian cancer cells^[1].

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

Cell Viability Assay^[1]

Cell Line:

Parental SKOV3, SKOV3 LIPA-knockout (LIPA-KO)
Concentration:

1 μM (RT-PCR/RT-qPCR); range of concentrations (cell viability assay)
Incubation Time:

0, 8, 16 h (RT-PCR/RT-qPCR); unspecified (cell viability assay)
Result:

Reduced cell viability and robustly induced XBP1 splicing, sXBP1 mRNA, and CHOP mRNA expression in parental SKOV3 cells following treatment.
Displayed markedly reduced sensitivity in SKOV3 LIPA-KO cells, with no significant induction of XBP1 splicing, sXBP1 mRNA, or CHOP mRNA expression.

In Vivo

ERX-208 (10 mg/kg; i.p.; 5 days per week for 15 consecutive days) reduces the ovarian cancer tumor burden by approximately 60% in orthotopic SCID mouse xenograft models, while also decreasing tumor weight and reducing the number of metastatic nodules, with no obvious systemic toxicity^[1].
ERX-208 (2.5-10 mg/kg; i.p.; once every three days; for a total of 11 days) dose-dependently inhibits the growth of OCa30 PDX tumors in SCID mice; among all groups, the 10 mg/kg group shows the greatest reduction in tumor weight, the most significant downregulation of Ki67 expression, and the most prominent upregulation of GRP78 expression, with no obvious systemic toxicity observed^[1].
ERX-208 (10 mg/kg; i.p.; once every three days; for 21 consecutive days) significantly inhibits the growth of OCa14 PDX tumors in SCID mice and reduces the final tumor weight, while downregulating the expression of Ki67 and upregulating the expression of GRP78 in tumor tissues, with no obvious systemic toxicity^[1].
ERX-208 (10 mg/kg; i.p.; once every three days; for a total of 39 days) significantly inhibits the growth of OCa10 PDX tumors in SCID mice and reduces the final tumor weight, while downregulating Ki67 expression, upregulating GRP78 expression and activating the endoplasmic reticulum stress pathway, with no obvious systemic toxicity^[1].

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

Animal Model:

SCID mice (8-week-old female; orthotopic xenograft model via intraperitoneal injection of ES2 GFP-Luciferase-expressing ovarian cancer cells)^[1]
Dosage:

10 mg/kg
Administration:

i.p.; 5 days per week for 15 consecutive days
Result:

Reduced ovarian cancer tumor burden by approximately 60% compared to vehicle controls.
Significantly decreased final tumor weight compared to vehicle controls.
Significantly reduced the number of peritoneal metastatic tumor nodules compared to vehicle controls.
Caused no significant changes in mouse body weight, indicating good tolerability.

Animal Model:

SCID mice (8-week-old female; ectopic OCa30 patient-derived xenograft model)^[1]
Dosage:

2.5 mg/kg; 5 mg/kg; 10 mg/kg
Administration:

i.p.; once every three days; for a total of 11 days
Result:

Inhibited tumor growth in a dose-dependent manner, with the most significant suppression at the 10 mg/kg dose.
Significantly lowered final tumor weights in all treated groups, with the greatest reduction at 10 mg/kg.
Decreased the proliferation marker Ki67 in a dose-dependent manner in tumor tissue.
Increased the endoplasmic reticulum stress marker GRP78 in a dose-dependent manner in tumor tissue.
Caused no significant changes in mouse body weight across all dosing groups.

Animal Model:

SCID mice (8-week-old female; ectopic OCa14 patient-derived xenograft model)^[1]
Dosage:

10 mg/kg
Administration:

i.p.; once every three days; for 21 consecutive days
Result:

Significantly inhibited tumor growth throughout the study period compared to vehicle controls.
Markedly decreased final tumor weight compared to vehicle controls.
Significantly decreased Ki67-positive proliferative cells in tumor tissue.
Significantly increased GRP78 expression in tumor tissue.
Caused no significant changes in mouse body weight.

Animal Model:

SCID mice (8-week-old female; ectopic OCa10 patient-derived xenograft model)^[1]
Dosage:

10 mg/kg
Administration:

i.p.; once every three days; for a total of 39 days
Result:

Significantly inhibited tumor growth kinetics compared to vehicle controls.
Significantly decreased final tumor weight compared to vehicle controls.
Significantly decreased Ki67-positive proliferative cells in tumor tissue.
Significantly increased GRP78 expression in tumor tissue.
Activated additional endoplasmic reticulum stress markers including p-eIF2α, p-PERK, and CHOP in tumor tissue.
Caused no significant changes in mouse body weight.

Chemical Information

CAS. Nr. 2440087-57-8
Molecular Weight 860.95
Formel C₄₇H₅₂N₆O₁₀
SMILES

OCCOC1=C([N+]([O-])=O)C=CC(C(NC(C(OCC(C)C)=C2)=CC=C2C(NC3=C(OCC(C)C)C=C(C(N[C@@H]4CC[C@@H](C(NC5=CN=C(C=CC=C6)C6=C5)=O)CC4)=O)C=C3)=O)=O)=C1
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Viswanadhapalli S, et al. Therapeutic optimization of LIPA targeting to induce endoplasmic reticulum stress and cell death in ovarian cancer. Oncogene. 2026;45(8):790-804. [Content Brief]

Calculators

Molaritätsrechner

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

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

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.

Keywords

100 mg

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