| Field | Specification |
|---|---|
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C16H12O3 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
HS-1793 is a Resveratrol analogue that shows antitumor activity across a range of cancer cell lines[1] and induces apoptosis in these cells[2]. It is supplied as an off-white to light yellow solid (C16H12O3, MW 252.26) at 99.26% purity.
Physical & Chemical Properties
| CAS Number | 927885-00-5 |
|---|---|
| Molecular Formula | C16H12O3 |
| Molecular Weight | 252.26 g/mol |
| Purity | 99.26% |
| Appearance | Solid |
| Color | Off-white to light yellow |
| SMILES | OC1=CC=C(C2=CC=C3C=C(O)C=CC3=C2)C(O)=C1 |
| Signaling Pathway | Apoptosis |
| Solubility | In Vitro: DMSO: 125 mg/mL (495.52 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 6 months; -20°C, 1 month. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 125 mg/mL (495.52 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
HS-1793 (0-100 μM; 24 h) suppresses the proliferation of MCF-7, MDA-MB-231 and HCT116 cells[1][2]. In MCF-7 and MDA-MB-231 cells, HS-1793 (0-50 μM; 4 h) inhibits hypoxia-induced HIF-1α protein independent of cell death, downregulates hypoxia-induced VEGF expression, and suppresses hypoxia-induced VEGF mRNA expression at the transcriptional level[1]. In HCT116 cells, 24 h of HS-1793 (0-100 μM) triggers apoptosis and G2/M cell cycle arrest and reduces Akt and ERK phosphorylation[2].
Cell Proliferation Assay[1]
| Cell Line | MCF-7, MDA-MB-231 and MCF-10A |
|---|---|
| Concentration | 0-100 μM |
| Incubation Time | 24 h |
| Result | Showed antiproliferation activity with IC50 values of 26.3±3.2, 48.2±4.2 and >100 μM against MCF-7, MDA-MB-231 and MCF-10A, respectively. |
Western Blot Analysis[1]
| Cell Line | MCF-7, MDA-MB-231 |
|---|---|
| Concentration | 12.5, 25 and 50 μM |
| Incubation Time | 4 h |
| Result | Downregulated HIF-1α expression in a concentration-dependent manner in both cell lines. |
RT-PCR[1]
| Cell Line | MCF-7, MDA-MB-231 |
|---|---|
| Concentration | 12.5, 25 and 50 μM |
| Incubation Time | 4 h |
| Result | Downregulated the expression of VEGF mRNA, with the more marked results observed in MDA-MB-231 cells. |
Cell Proliferation Assay[2]
| Cell Line | HCT116 |
|---|---|
| Concentration | 12.5, 25, 50 and 100 μM |
| Incubation Time | 1, 2 and 4 days |
| Result | Significantly reduced the cell viability concentration- and time-dependently. Significantly suppressed proliferation of colon cancer cell line HCT116. |
Apoptosis Analysis[2]
| Cell Line | HCT116 |
|---|---|
| Concentration | 12.5, 25, 50 and 100 μM |
| Incubation Time | 24 h |
| Result | Induced cell apoptosis in a dose-dependent manner. Caused chromatin condensation and fragmentation. |
Western Blot Analysis[2]
| Cell Line | HCT116 |
|---|---|
| Concentration | 12.5, 25, 50 and 100 μM |
| Incubation Time | 24 h |
| Result | Effectively induced the reduction of pro-caspase-8 and pro-caspase-3 at 100 μM. Activated caspase-8 and caspase-3. Caused the PARP cleavage. Slightly downregulated the level of antiapoptotic protein Bcl-2 at 100 μM. Promoted an increase in the release of cytochrome c from the mitochondria into the cytosol. Decreased the expression of G2/M cell cycle regulatory protein cyclin B1, Cdc2 and Cdc25C. Decreased the level of CDK4 and CDK6. Decreased Akt phosphorylation and reduced total Akt at high-concentration. Decreased the phosphorylation of ERK1/2 without affecting the protein level. |
Cell Cycle Analysis[2]
| Cell Line | HCT116 |
|---|---|
| Concentration | 12.5, 25 and 50 μM |
| Incubation Time | 24 h |
| Result | Induced the accumulation of cells in the G2/M phase in a concentration-dependent manner. |
In Vivo
Given i.p. twice a week for 4 weeks, HS-1793 (5 and 10 mg/kg) significantly inhibits the growth of MDA-MB-231 xenograft tumors in a dose-dependent manner and relatively hampers angiogenesis, without toxicity[1].
| Animal Model | Five-week-old female BALB/c nude mice injected with MDA-MB-231 cells[1] |
|---|---|
| Dosage | 5 mg/kg and 10 mg/kg (dissolved in PBS containing 0.1% v/v dimethyl sulfoxide (DMSO)) |
| Administration | Intraperitoneal injection, twice a week, 4 weeks |
| Result | Significantly inhibited MDA-MB-231 xenograft tumor growth in a dose-dependent manner with non-toxicity. Significantly lowered Ki-67 (a proliferation marker) and CD31 expression. Successfully suppressed the expression of HIF-1α and VEGF in tumor tissues. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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