Aristoforin
Aristoforin, a hypericin derivative, inhibits the activities of SIRT1 and SIRT2. Aristoforin induces G1 phase cell cycle arrest, scavenges hydroxyl free radicals, and exhibits protective activity against Fe2+-induced DNA breakage. Aristoforin can be used in studies related to breast cancer and colon adenocarcinoma.
For research use only. We do not sell to patients.
- CAS No.: 849215-53-8
- Formula: C37H54O6
- Molecular Weight:594.82
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
In Vitro
Aristoforin (24 h) potently inhibits primary human umbilical vein endothelial cell proliferation with a mean IC50 of 3.14 μM[1].
Aristoforin (24 h) potently inhibits primary human dermal lymphatic endothelial cell proliferation with a mean IC50 of 2.54 μM, and completely blocks proliferation at 5 μM[1].
Aristoforin (24 h) potently inhibits primary human lung lymphatic endothelial cell proliferation with a mean IC50 of 2.63 μM[1].
Aristoforin (10-50 μM; 24 h) induces dose-dependent apoptosis in primary human dermal lymphatic endothelial cells, with significant effects observed at concentrations of 10 μM and above, and exhibits greater proapoptotic potency than hyperforin[1].
Aristoforin (5-30 μM; 48 h) induces G1 phase cell cycle arrest in primary human dermal lymphatic endothelial cells at 5 μM, and induces apoptosis (evidenced by increased sub-G1 cells) at 30 μM[1].
Aristoforin (30 μM; 48 h) activates the intrinsic apoptosis pathway in primary human dermal lymphatic endothelial cells at 30 μM, as shown by activation of caspase-3 and caspase-9 without caspase-8 activation[1].
Aristoforin (20 μM; 20 min at 37°C) induces a rapid loss of mitochondrial membrane potential in primary human dermal lymphatic endothelial cells[1].
Aristoforin (1-5 μM; 16 h) alters MRP1, MRP2, BCRP, and P-gp protein levels in human colon adenocarcinoma HT-29 cells in a time- and light-dependent manner, including decreased MRP2 at T0- and T6+, increased MRP1 at T0-, and increased P-gp at T6+ and T6-[2].
Aristoforin (1-5 μM; 16 h) alters CYP3A4 protein levels in human colon adenocarcinoma HT-29 cells in vitro in a concentration-, time-, and light-dependent manner, including increased levels at T0-, T6-, and T6+ (1 μM), and decreased levels at T0+ (5 μM)[2].
Aristoforin (1-5 μM; 16 h) induces BCRP mRNA expression at T0- in human colon adenocarcinoma HT-29 cells[2].
Aristoforin (1-5 μM; 16 h) modulates CYP3A4 mRNA expression in human colon adenocarcinoma HT-29 cells in vitro in a concentration-, time-, and light-dependent manner, including induction at T0+ (1 μM) and T6+ (5 μM), and reduction at T6-[2].
Aristoforin (5-10 μM; 30 min) significantly decreases BCRP activity in human colon adenocarcinoma HT-29 cells, with no significant effect on MRP1 or MRP2 activity[2].
Aristoforin (10 μM; 16 h) significantly decreases CYP3A4 activity in both human colon adenocarcinoma HT-29 cells and Oxaliplatin (HY-17371)-resistant HT-29-OxR cells, independent of light activation[2].
Aristoforin (0.01-10 mM; 25 min) exhibits concentration-dependent DPPH radical scavenging activity, with 5.76%, 12.03%, 17.89%, and 28.02% scavenging at 0.01, 0.1, 1, and 10 mM respectively[3].
Aristoforin (0.01-10 mM; 20 min at 50°C) exhibits very low reducing power, with absorbance values of 0.002, 0.002, 0.068, and 0.085 at 0.01, 0.1, 1, and 10 mM respectively[3].
Aristoforin (0.01-10 mM; 10 min) does not chelate ferrous ions at concentrations ranging from 0.01 to 10 mM[3].
Aristoforin (0.01-1 mM; 90 min at 25°C) exhibits concentration-dependent hydroxyl radical scavenging activity, with 18.18 ± 6.54%, 33.0 ± 2.75%, and 55.84 ± 8.21% scavenging at 0.01, 0.1, and 1 mM respectively[3].
Aristoforin (1-5 μM) at 5 μM, when used as a 16 h pre-incubation followed by 50 nM Hypericin (HY-N0453)-mediated PDT, significantly enhances apoptosis in HT-29 colon adenocarcinoma cells[4].
Aristoforin (1-5 μM) at 5 μM, when used as a 16 h pre-incubation followed by 50 nM Hypericin-mediated PDT, normalizes the cell cycle distribution of HT-29 colon adenocarcinoma cells at 24 h post-PDT, counteracting the S-phase accumulation induced by PDT alone[4].
Aristoforin (1-5 μM) at 5 μM, when used as a 16 h pre-incubation followed by 50 nM hypericin-mediated PDT, significantly suppresses MMP2 and MMP9 expression in HT-29 colon adenocarcinoma cells at 6 h post-PDT[4].
Aristoforin (1-5 μM) at 5 μM, when used as a 16 h pre-incubation followed by 50 nM hypericin-mediated PDT, drastically reduces cellular adhesivity of HT-29 colon adenocarcinoma cells[4].
Aristoforin (1-5 μM) at 5 μM, when used as a 16 h pre-incubation followed by 50 nM hypericin-mediated PDT, potently suppresses clonogenic survival of HT-29 colon adenocarcinoma cells[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:human colon adenocarcinoma HT-29 cells
-
Concentration:1 μM; 5 μM
-
Incubation Time:16 h
-
Result:Decreased MRP2 and BCRP protein levels, and increased MRP1 protein levels at T0- (dark, immediate post-treatment).
Increased MRP2 protein levels, decreased BCRP protein levels, and decreased MRP1 protein levels at T0+ (post-PDT, immediate post-treatment).
Increased MRP2, BCRP, and P-gp protein levels at T6- (dark, 6 h post-treatment).
Decreased MRP2 and BCRP protein levels, and increased P-gp protein levels at T6+ (post-PDT, 6 h post-treatment).\nIncreased CYP3A4 protein levels 2.15-fold (1 μM) and 2.55-fold (5 μM) relative to control at T0- (dark, immediate post-treatment).
Decreased CYP3A4 protein levels 0.74-fold relative to control at T0+ (post-PDT, immediate post-treatment) at 5 μM.
Increased CYP3A4 protein levels 1.11-fold (1 μM) and 1.21-fold (5 μM) relative to control at T6- (dark, 6 h post-treatment).
Increased CYP3A4 protein levels 1.98-fold relative to control at T6+ (post-PDT, 6 h post-treatment) at 1 μM.
-
Cell Line:HT-29 colon adenocarcinoma cells
-
Concentration:1 μM; 5 μM
-
Incubation Time:16 h
-
Result:Partially reversed the S-phase accumulation caused by PDT alone, restoring cell cycle distribution to levels similar to untreated control cells when combined with 50 nM hypericin-mediated PDT.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Wistar rats (female)[1]
-
Dosage:2 mM (delivered as 100 μL per injection)
-
Administration:s.c.; daily; 14 days
-
Result:Reduced peritumoral podoplanin-positive lymphatic vessel density significantly compared to DMSO control.
Left tumor volumes equivalent to control groups at the time of sacrifice.
Chemical Information
-
CAS No. 849215-53-8
-
Molecular Weight 594.82
-
Formula C37H54O6
-
SMILES
CC(C)C([C@@]12[C@@](C)([C@H](C[C@@](C1=O)(C(OCC(O)=O)=C(C2=O)C/C=C(C)\C)C/C=C(C)\C)C/C=C(C)\C)CC/C=C(C)/C)=O
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
-
BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
-
Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
-
Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Purity & Documentation
References
[1]. Rothley M, et al. Hyperforin and aristoforin inhibit lymphatic endothelial cell proliferation in vitro and suppress tumor-induced lymphangiogenesis in vivo. Int J Cancer. 2009;125(1):34-42. [Content Brief]
[2]. Šemeláková M, et al. Drug membrane transporters and CYP3A4 are affected by hypericin, hyperforin or aristoforin in colon adenocarcinoma cells. Biomed Pharmacother. 2016;81:38-47. [Content Brief]
[3]. Ševčovičová A, et al. DNA-protective activities of hyperforin and aristoforin. Toxicol In Vitro. 2015;29(3):631-637. [Content Brief]
[4]. Šemeláková M, et al. The pro-apoptotic and anti-invasive effects of hypericin-mediated photodynamic therapy are enhanced by hyperforin or aristoforin in HT-29 colon adenocarcinoma cells. J Photochem Photobiol B. 2012;117:115-125. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Aristoforin Related Classifications
HY-133849 Related Classifications
Powered by Bioz