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^[1][2][3][4].

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.

Aristoforin (2 mM; s.c.; daily; 14 days) significantly suppresses tumor-induced lymphangiogenesis in MT-450 breast tumor-bearing female Wistar rats, reducing peritumoral lymphatic vessel density with relative to DMSO control, without altering tumor volume at the study endpoint^[1].

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

594.82

C₃₇H₅₄O₆

849215-53-8

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Room temperature in continental US; may vary elsewhere.

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

• [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]