ERX-208 (6 days) effectively reduced cell viability in all five ovarian cancer cell subtypes, with an IC50 of approximately 100 nM, and exhibited extremely low cytotoxicity to normal ovarian surface epithelial cells [1]. ERX-208 significantly inhibited the long-term proliferative capacity of ovarian cancer cells, as confirmed by colony formation assays [1]. ERX-208 (500 nM) induced caspase-dependent apoptosis in ovarian cancer cells, but no ferroptosis or necroptosis was observed [1]. ERX-208 (1 μM; 0–48 h) significantly activated endoplasmic reticulum stress responses at the transcriptional, post-transcriptional, and ultrastructural levels in various ovarian cancer models [1]. ERX-208 (1 μM; 0–16 h)-mediated endoplasmic reticulum stress responses and cytotoxicity in SKOV3 ovarian cancer cells were dependent on LIPA expression [1]. ERX-208 (22 h) effectively inhibited the invasive capacity of ascites-derived ovarian cancer cells [1].

ERX-208 (10 mg/kg; intraperitoneal injection; 5 days a week for 15 consecutive days) reduced the tumor burden of ovarian cancer by about 60% in the orthotopic SCID mouse xenograft model, while also reducing tumor weight and the number of metastatic nodules, and no obvious systemic toxicity was observed [1]. ERX-208 (2.5-10 mg/kg; intraperitoneal injection; every three days for 11 days) inhibited the growth of OCa30 PDX tumors in SCID mice in a dose-dependent manner; among all dose groups, the 10 mg/kg group had the largest reduction in tumor weight, the most significant downregulation of Ki67 expression, and the most significant upregulation of GRP78 expression, and no obvious systemic toxicity was observed [1]. ERX-208 (10 mg/kg; intraperitoneal injection; every three days for 21 consecutive days) significantly inhibited the growth of OCa14 PDX tumors in SCID mice, reduced the final tumor weight, downregulated Ki67 expression in tumor tissue, upregulated GRP78 expression, and had no obvious systemic toxicity [1]. ERX-208 (10 mg/kg; intraperitoneal injection; once every three days; for a total of 39 days) significantly inhibited the growth of OCa10 PDX tumors in SCID mice, reduced the final tumor weight, downregulated the expression of Ki67, upregulated the expression of GRP78, and activated the endoplasmic reticulum stress pathway, without significant systemic toxicity [1].

Cell viability assay [1]
Cell Types: Parental SKOV3 cells, SKOV3 LIPA knockout (LIPA-KO) cells
Tested Concentrations: 1 μM (RT-PCR/RT-qPCR); Concentration range (cell viability assay)
Incubation Duration: 0, 8, 16 hours (RT-PCR/RT-qPCR); Not specified (cell viability assay)
Experimental Results: After treatment, the viability of parental SKOV3 cells decreased, and the expression of XBP1 splicing, sXBP1 mRNA, and CHOP mRNA was significantly upregulated. The sensitivity of SKOV3 LIPA-KO cells was significantly reduced, and the expression of XBP1 splicing, sXBP1 mRNA, and CHOP mRNA was not significantly upregulated.

Animal/Disease Models:SCID mice (8-week-old females; orthotopic xenograft model established by intraperitoneal injection of ES2 ovarian cancer cells expressing GFP-luciferase) [1]
Doses: 10 mg/kg
Route of Administration: Intraperitoneal injection; 5 days a week for 15 consecutive days
Experimental Results: Compared with the vector control group, the ovarian cancer tumor burden was reduced by approximately 60%. Compared with the vector control group, the final tumor weight was significantly reduced. Compared with the vector control group, the number of peritoneal metastatic tumor nodules was significantly reduced. No significant change in mouse body weight was observed, indicating good tolerability.

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Animal/Disease Models:SCID mice (8-week-old females; ectopic OCa30 patient-derived xenograft model) [1]
Doses: 2.5 mg/kg; 5 mg/kg; 10 mg/kg
Route of Administration: Intraperitoneal injection; once every three days; for a total of 11 days
Experimental Results: Tumor growth was inhibited in a dose-dependent manner, with the 10 mg/kg dose group showing the most significant inhibitory effect. The final tumor weight was significantly reduced in all treatment groups, with the 10 mg/kg dose group showing the largest reduction. The proliferation marker Ki67 in tumor tissue decreased in a dose-dependent manner. The endoplasmic reticulum stress marker GRP78 in tumor tissue increased in a dose-dependent manner. The body weight of mice in all dose groups did not change significantly.

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Animal/Disease Models:SCID mice (8-week-old females; ectopic OCa14 patient-derived xenograft model) [1]
Doses: 10 mg/kg
Route of Administration: Intraperitoneal injection; every three days for 21 consecutive days
Experimental Results: Tumor growth was significantly inhibited throughout the study period compared with the vector control group. Tumor weight was significantly reduced compared with the vector control group. Ki67-positive proliferating cells were significantly reduced in tumor tissue. GRP78 expression was significantly increased in tumor tissue. No significant change in mouse body weight was observed.

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Animal/Disease Models:SCID mice (8-week-old females; ectopic OCa10 patient-derived xenograft model) [1]
Doses: 10 mg/kg
Route of Administration: Intraperitoneal injection; every three days for a total of 39 days
Experimental Results: Significantly inhibited tumor growth kinetics compared with the vector control group. Significantly reduced final tumor weight compared with the vector control group. Significantly reduced the number of Ki67-positive proliferating cells in tumor tissue. Significantly increased the expression of GRP78 in tumor tissue. Activated other endoplasmic reticulum stress markers in tumor tissue, including p-eIF2α, p-PERK, and CHOP. No significant change in mouse body weight.

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

C47H52N6O10

860.95

2440087-57-8

Typically exists as solids at room temperature

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

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)