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Trifolirhizin is a pterocarpan flavonoid found in the roots of Sophora flavescens. Trifolirhizin is a tyrosinase inhibitor with an IC50 value of 506.77 μM. Trifolirhizin reduces intracellular melanin production and modulates multiple signaling pathways including NFκB-MAPK, AMPK/mTOR, PI3K/Akt, MAPK-NFATc1 and EGFR-MAPK. Trifolirhizin targets biological molecules including PTK6 and COX-2, inhibits the activities of hyaluronidase, collagenase and elastase, induces apoptosis, autophagy and cell cycle arrest, and suppresses the proliferation, migration and invasion of cancer cells. Trifolirhizin exerts diverse pharmacological effects including anti-inflammatory, anti-asthmatic, bone-protective, renoprotective, antibacterial, antifungal, hepatoprotective, antiplatelet, estrogenic and wound-healing activities. Trifolirhizin can be used to investigate a broad range of malignant, inflammatory, metabolic and infectious disorders.
For research use only. We do not sell to patients.
Trifolirhizin is a pterocarpan flavonoid found in the roots of Sophora flavescens. Trifolirhizin is a tyrosinase inhibitor with an IC50 value of 506.77 μM. Trifolirhizin reduces intracellular melanin production and modulates multiple signaling pathways including NFκB-MAPK, AMPK/mTOR, PI3K/Akt, MAPK-NFATc1 and EGFR-MAPK. Trifolirhizin targets biological molecules including PTK6 and COX-2, inhibits the activities of hyaluronidase, collagenase and elastase, induces apoptosis, autophagy and cell cycle arrest, and suppresses the proliferation, migration and invasion of cancer cells. Trifolirhizin exerts diverse pharmacological effects including anti-inflammatory, anti-asthmatic, bone-protective, renoprotective, antibacterial, antifungal, hepatoprotective, antiplatelet, estrogenic and wound-healing activities. Trifolirhizin can be used to investigate a broad range of malignant, inflammatory, metabolic and infectious disorders[1][2][3].
Trifolirhizin exerts anti-inflammatory effects in LPS-stimulated mouse J774A.1 macrophages by downregulating TNF-α, IL-6, and COX-2 expression[1]. Trifolirhizin (50-100 μg/mL) inhibits wound-healing related enzymes hyaluronidase, collagenase, and elastase, with maximum inhibition observed at 100 μg/mL[1]. Trifolirhizin (1-500 μg/mL; 12.5-50 μM) exhibits skin-whitening activity by inhibiting tyrosinase (IC50 = 506.77 μM) and reducing melanin production in IBMX-induced B16 melanoma cells (IC50 = 36 μM)[1]. Trifolirhizin (10-40 μM) inhibits RANKL-induced osteoclast formation and bone resorption in mouse BMMs at 10, 20, and 40 μM by downregulating NFATc1 and osteoclast marker genes[1]. Trifolirhizin (270-360 μM) inhibits proliferation and induces apoptosis in HL-60 human leukemia cells, while sparing normal lymphocytes at 270-360 μM[1]. Trifolirhizin (5-250 μM) exerts dose-dependent antiproliferative activity in A2780 human ovarian cancer cells (effective at ≥50 μM) and H23 human lung cancer cells (effective at 250 μM)[1]. Trifolirhizin (20-40 μg/mL) inhibits proliferation and induces apoptosis in MKN45 human gastric cancer cells (IC50 = 33.27 μg/mL) via cell cycle arrest and modulation of EGFR-MAPK signaling, while exhibiting low toxicity to normal kidney and liver cell lines[1]. Trifolirhizin induces autophagy-dependent apoptosis in HCT116 and SW620 human colorectal cancer cells by activating the AMPK/mTOR signaling pathway[1]. Trifolirhizin inhibits proliferation, migration, and invasion of 6-10 B and HK1 human nasopharyngeal carcinoma cells, with IC50 values of 83.67 μmol/L and 33.21 μmol/L at 72 h, by suppressing the PI3K/Akt signaling pathway[1]. Trifolirhizin (12.5-100 μg/mL; 50.0 μg/mL combined with sorafenib) exhibits dose-dependent antiproliferative activity in MHCC97H, MHCC97L, and HepG2 human hepatocellular carcinoma cells, and synergistically enhances the anticancer effects of sorafenib by inducing apoptosis and modulating cell cycle and signaling pathways[1]. Trifolirhizin (0.005-2 mg/mL) inhibits proliferation and induces apoptosis in C666-1 human nasopharyngeal carcinoma cells by targeting PTK6 and modulating autophagy-related markers[1]. Trifolirhizin (100 μg/mL) exhibits antibacterial activity against Helicobacter pylori at 100 μg/mL[1]. Trifolirhizin (10-25 μM; 2 h pre-incubation, 24 h LPS treatment) dose-dependently inhibits LPS-induced TNF-α and IL-6 mRNA expression in mouse J774A.1 macrophages, with complete inhibition of TNF-α mRNA observed at 25 μM[2]. Trifolirhizin (10-25 μM) dose-dependently inhibits LPS-induced TNF-α protein production in mouse J774A.1 macrophages, with no significant effect on IL-6 protein production[2]. Trifolirhizin (100-200 μM; 2 h pre-incubation, 24 h LPS treatment) dose-dependently inhibits LPS-induced COX-2 protein expression in mouse J774A.1 macrophages, with 14% inhibition at 100 μM and 28% inhibition at 200 μM[2]. Trifolirhizin (0-250 μM; 24 h) dose-dependently inhibits proliferation of human A2780 ovarian cancer cells (with significant 50% growth inhibition at 100 μM) and human H23 lung cancer cells (with significant activity only at 250 μM) after 24 h of incubation[2]. Trifolirhizin (10-40 μM; 6 h) accelerates autophagy flux in HCT116 and SW620 human colorectal cancer cells, as evidenced by altered autophagy marker protein expression, formation of autophagic vacuoles, and increased autophagosome and autophagolysosome formation[3]. Trifolirhizin (10-40 μM) activates the AMPK/mTOR signaling pathway in HCT116 and SW620 human colorectal cancer cells, which is essential for its induction of autophagy[3]. Trifolirhizin (10-45 μM; 48 h) induces caspase-mediated extrinsic pathway apoptosis in HCT116 and SW620 human colorectal cancer cells, reducing cell viability and colony formation[3]. Trifolirhizin (20 μM)-induced apoptosis in HCT116 and SW620 human colorectal cancer cells is dependent on AMPK activation and autophagy induction, with co-localization of autophagic and apoptotic markers confirming autophagy-mediated cell death[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Significantly inhibited LPS-induced increases in TNF-α and IL-6 mRNA expression in a dose-dependent manner. Completely inhibited the LPS-induced increase of TNF-α mRNA levels at 25 μM.
Dose-dependently inhibited LPS-stimulated COX-2 protein expression. Suppressed LPS-induced COX-2 protein production by 14% at 100 μM. Suppressed LPS-induced COX-2 protein production by 28% at 200 μM, based on the density ratio of COX-2 versus β-actin.
human A2780 ovarian cancer cells, human H23 lung cancer cells
Concentration:
0-250 μM
Incubation Time:
24 h
Result:
Dose-dependently suppressed the proliferation of both A2780 ovarian and H23 lung cancer cells. Showed no antiproliferative activity at concentrations less than 50 μM in either cell line. Achieved significant 50% growth inhibition in A2780 cells at 100 μM. Showed significant antiproliferative activity in H23 cells only at 250 μM.
6 h (transmission electron microscopy, Ad-mCherry-GFP-LC3B fluorescent assay)
Result:
Caused dose-related accumulation of LC3B-I and LC3B-II, and increased the LC3B-II/I expression ratio. Downregulated SQSTM-1 protein expression in both cell lines. Decreased SQSTM1 content while increased LC3B-II and poly-ubiquitin aggregated in detergent-insoluble fractions. Revealed autophagic vacuoles (double-membrane compartments with lamellar structures) in treated cells. Showed increased green (autophagosomes) and red (autophagolysosomes) dots, indicating accelerated autophagy flux. Impaired trifolirhizin-induced autophagy flux when co-treated with autophagy inhibitors.
Reduced cell viability in a dose-dependent manner. Inhibited long-term colony formation. Induced both early and late apoptosis in both cell lines. Showed unchanged cleaved caspase-9 and cytochrome c expression, but increased cleaved poly ADP-ribose polymerase, cleaved caspase-3, and cleaved caspase-8 expression. Decreased trifolirhizin's cytotoxicity when co-treated with Z-VAD-FMK.
Trifolirhizin (7.5 mg/kg; daily; 5 days prior to carbon tetrachloride exposure and continued for study duration) exerts hepatoprotective effects in carbon tetrachloride-intoxicated Wistar rats by normalizing liver enzyme and bilirubin levels and restoring liver non-protein sulfhydryl groups[1]. Trifolirhizin (20 mg/kg; single treatment) exhibits strong estrogenic activity in young female Wistar rats, increasing uterine weight by over 90%[1]. Trifolirhizin (4.5 mg/kg; single treatment) reduces carrageenan-induced hind paw edema in Wistar rats by 35%[1]. Trifolirhizin (10-20 mg/kg; intraperitoneal injection; daily; 6 weeks) protects against ovariectomy-induced bone loss in female C57BL/6J mice by reducing osteoclast number and bone resorption[1]. Trifolirhizin (5-10 mg/kg; periosteal injection; days 2, 4, 6, and 8 post-LPS exposure) prevents LPS-induced inflammatory osteolysis in male C57BL/6J mice in vivo in a dose-dependent manner by reducing osteoclast formation and bone destruction[1]. Trifolirhizin (1-3 mg/kg; daily; 21 days) inhibits gastric tumor growth in BALB/C nude mice, reducing tumor weight and increasing tumor cell apoptosis while decreasing proliferation[1]. Trifolirhizin (10 mg/kg; once every 3 days; 21 days) suppresses colorectal xenograft tumor growth in C57BL/6 mice by activating the AMPK/mTOR pathway to induce autophagy and caspase-mediated extrinsic apoptosis[1]. Trifolirhizin (40 mg/kg; every other day; 14 days) inhibits nasopharyngeal carcinoma xenograft tumor growth in male nude mice without causing damage to normal kidney or liver tissue[1]. Trifolirhizin (12.5-50 mg/kg; intraperitoneal injection; single dose) exerts anti-ulcerative colitis effects in DSS-induced C57BL/6 mice by regulating Th17/Treg balance and suppressing the NLRP3 inflammasome via the AMPK-TXNIP pathway[1]. Trifolirhizin (12.5-50 mg/kg; daily; 3 weeks) relieves renal injury in male db/db diabetic nephropathy mice by inducing autophagy, inhibiting oxidative stress, and regulating the PI3K/AKT/mTOR pathway[1]. Trifolirhizin (2-5 mg/kg; daily) mitigates ovalbumin-induced asthma in neonatal Sprague Dawley rats in vivo in a dose-dependent manner by reducing pulmonary inflammation and tissue damage via modulation of the NF-κB pathway[1]. Trifolirhizin (10 mg/kg) significantly suppresses colorectal cancer xenograft growth in C57BL/6 mice, activates the AMPK/mTORautophagy pathway, and induces extrinsic apoptosis in tumor cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
daily; 5 days prior to carbon tetrachloride exposure and continued for study duration
Result:
Significantly reduced serum levels of SGOT, SGPT, ALP, and total bilirubin. Increased liver non-protein sulfhydryl group levels compared to the carbon tetrachloride-only group.
Animal Model:
C57BL/6J mice (female; ovariectomy-induced bone loss)[1]
Dosage:
10 mg/kg; 20 mg/kg
Administration:
intraperitoneal injection; daily; 6 weeks
Result:
Reduced ovariectomy-induced bone loss. Decreased number of TRAP-positive osteoclasts in tibial tissue. High-dose treatment significantly recovered trabecular bone structure on μCT analysis.
Animal Model:
C57BL/6J mice (male; LPS-induced cranial bone inflammation and bone loss)[1]
Dosage:
5 mg/kg; 10 mg/kg
Administration:
periosteal injection; days 2, 4, 6, and 8 post-LPS exposure
Result:
Dose-dependently reduced LPS-induced osteolysis. Increased bone volume/tissue volume (BV/TV). Decreased bone destruction area. Reduced number of TRAP-positive osteoclasts and IL-1β-positive area in cranial cap tissue.
Dose-dependently reduced disease activity index (DAI). Increased colon length in 25 and 50 mg/kg groups. Improved body weight. Downregulated mRNA and protein expression of TNF-α, IL-6, and IL-1β in colon tissue. Suppressed p-NF-κB/NF-κB and RORγt protein expression. Increased Foxp3 expression. Reduced Th17 (CD4+ IL17+) cells and increased Treg (CD4+ CD25+ Foxp3+) cells in mesenteric lymph nodes and spleen. Suppressed NLRP3 inflammasome components (NLRP3, caspase 1, ASC). Regulated the AMPK-TXNIP pathway by reducing p-AMPK/AMPK and increasing TXNIP.
Animal Model:
db/db mice (male; spontaneous type 2 diabetes-induced renal injury)[1]
Dosage:
12.5 mg/kg; 25 mg/kg; 50 mg/kg
Administration:
daily; 3 weeks
Result:
Reduced body and renal weight. Decreased fasting blood glucose. Improved renal histopathology (reduced glomerular hypertrophy, tubular basement membrane thickening, mesangial matrix expansion). Reduced serum BUN and creatinine. Suppressed renal tissue apoptosis via TUNEL assay. Decreased MDA and ROS levels. Increased SOD levels. Upregulated LC3II and Beclin1 expression. Downregulated p62, p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR expression in renal tissue.
Animal Model:
Sprague Dawley rats (neonatal; ovalbumin-induced pulmonary inflammation and tissue damage)[1]
Dosage:
2 mg/kg; 4 mg/kg; 5 mg/kg
Administration:
daily
Result:
Dose-dependently reduced serum IgE levels. Suppressed histological scores (reduced tissue damage, inflammatory cell aggregation, and pulmonary edema). Downregulated lung Muc5AC and Muc5B gene expression. Reduced BALF levels of TNF-α, ICAM-1, IL-4, IL-5, and IL-13. Upregulated lung IκBα protein expression.
DMSO : 100 mg/mL (224.01 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.2401 mL
11.2007 mL
22.4014 mL
5 mM
0.4480 mL
2.2401 mL
4.4803 mL
10 mM
0.2240 mL
1.1201 mL
2.2401 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (5.60 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (5.60 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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