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23-Hydroxybetulinic acid (Anemosapogenin) is an orally active triterpenoid with broad-spectrum anticancer activity. 23-Hydroxybetulinic acid reduces the levels of Bcl-2 and survivin, elevates the level of Bax, promotes the cleavage/activation of caspase-3 and caspase-9, and induces apoptosis via the endogenous mitochondrial pathway involving cytochrome C release and mitochondrial membrane potential disruption. 23-Hydroxybetulinic acid arrests the cell cycle at S and G1 phases, inhibits cancer cell proliferation, blocks the MAPK signaling pathway, regulates MMP2, and induces autophagic apoptosis by upregulating beclin-1. 23-Hydroxybetulinic acid inhibits the activity and efflux function of P-gp, increases the intracellular accumulation of chemotherapeutic drugs, and synergistically enhances cytotoxicity with Doxorubicin (HY-15142). 23-Hydroxybetulinic acid inhibits the phosphorylation and nuclear translocation of STAT6, blocks M2 macrophage polarization, and reduces M2 macrophage-mediated apoptosis resistance of colon cancer cells. 23-Hydroxybetulinic acid can be used in related studies on chronic myeloid leukemia, hepatocellular carcinoma, sarcoma 180, multidrug-resistant breast cancer, leukemia, Doxorubicin-induced cardiotoxicity, and colorectal cancer.
For research use only. We do not sell to patients.
23-Hydroxybetulinic acid (Anemosapogenin) is an orally active triterpenoid with broad-spectrum anticancer activity. 23-Hydroxybetulinic acid reduces the levels of Bcl-2 and survivin, elevates the level of Bax, promotes the cleavage/activation of caspase-3 and caspase-9, and induces apoptosis via the endogenous mitochondrial pathway involving cytochrome C release and mitochondrial membrane potential disruption. 23-Hydroxybetulinic acid arrests the cell cycle at S and G1 phases, inhibits cancer cell proliferation, blocks the MAPK signaling pathway, regulates MMP2, and induces autophagic apoptosis by upregulating beclin-1. 23-Hydroxybetulinic acid inhibits the activity and efflux function of P-gp, increases the intracellular accumulation of chemotherapeutic drugs, and synergistically enhances cytotoxicity with Doxorubicin (HY-15142). 23-Hydroxybetulinic acid inhibits the phosphorylation and nuclear translocation of STAT6, blocks M2 macrophage polarization, and reduces M2 macrophage-mediated apoptosis resistance of colon cancer cells. 23-Hydroxybetulinic acid can be used in related studies on chronic myeloid leukemia, hepatocellular carcinoma, sarcoma 180, multidrug-resistant breast cancer, leukemia, Doxorubicin-induced cardiotoxicity, and colorectal cancer[1][2][3][4][5][6][7].
23-Hydroxybetulinic acid (0-300 μM; 48 h) potently inhibits proliferation of human chronic myelogenous leukemia K562 cells (IC50 = 39.9 μM) and exhibits lower cytotoxicity against B16, HeLa, and HUVEC cells[1]. 23-Hydroxybetulinic acid (0-80 μM; 24 h) induces concentration-dependent S phase cell cycle arrest in human chronic myelogenous leukemia K562 cells after 24 h of treatment, with 80 μM HBA increasing S phase cells to 52.34%[1]. 23-Hydroxybetulinic acid (20-80 μM; 24 h) induces concentration-dependent apoptosis in human chronic myelogenous leukemia K562 cells after 24 h of treatment, as detected by Hoechst33342/PI dual staining[1]. 23-Hydroxybetulinic acid (20-80 μM; 24 h) significantly disrupts mitochondrial membrane potential in human chronic myelogenous leukemia K562 cells after 24 h of treatment, with 80 μM HBA reducing the red/green fluorescence ratio to 0.38[1]. 23-Hydroxybetulinic acid (10-80 μM; 24 h) triggers the intrinsic (mitochondrial) apoptosis pathway in human chronic myelogenous leukemia K562 cells after 24 h of treatment, via concentration-dependent modulation of pro- and anti-apoptotic proteins and activation of caspases[1]. 23-Hydroxybetulinic acid (1.25-20 μM; 48-72 h) inhibits viability of Huh-7, Hep3B, and Li-7 human HCC cells in a time- and concentration-dependent manner, with the strongest effect in Huh-7 cells at 20 μM for 72 h[2]. 23-Hydroxybetulinic acid (1.25-20 μM; 2-3 weeks) inhibits colony formation of Huh-7, Hep3B, and Li-7 human HCC cells over 2-3 weeks, with the strongest effect in Huh-7 cells[2]. 23-Hydroxybetulinic acid (5-20 μM; 48 h) promotes apoptosis of human HCC Huh-7 cells after 48 h in a concentration-dependent manner, and this effect is reversed by Bcl-2 overexpression[2]. 23-Hydroxybetulinic acid (5-20 μM) modulates apoptosis-related protein expression in human HCC Huh-7 cells, upregulating Bax and downregulating Bcl-2 and cleaved caspase-3 in a concentration-dependent manner[2]. 23-Hydroxybetulinic acid (5-20 μM) modulates migration/invasion and MAPK pathway-related protein expression in human HCC Huh-7 cells, decreasing MMP2, MMP9, p-MEK1/2, and p-ERK1/2 while increasing TIMP2 in a concentration-dependent manner[2]. 23-Hydroxybetulinic acid (5-20 μM; 48 h) inhibits migration invasionof human HCC Huh-7 cells after 48 h in a concentration-dependent manner[2]. 23-Hydroxybetulinic acid (48 h) dose-dependently inhibits the growth of NCI-H460, SGC7901, HepG2, and sarcoma 180 cells with average IC50 values of 49.2 μM, 49.1 μM, 306.4 μM, and 28.0 μM, respectively[3]. 23-Hydroxybetulinic acid (0.2-20 μM; 48 h) dose-dependently increases ADR cytotoxicity to P-gp-overexpressing MCF-7/ADR human breast carcinoma cells, reducing cell survival[4]. 23-Hydroxybetulinic acid (0.2-20 μM; 48 h) dose-dependently increases VCR cytotoxicity to P-gp-overexpressing MCF-7/ADR human breast carcinoma cells, reducing cell survival[4]. 23-Hydroxybetulinic acid (2-20 μM) dose-dependently increases ADR-induced apoptosis in P-gp-overexpressing MCF-7/ADR human breast carcinoma cells[4]. 23-Hydroxybetulinic acid (0.2-20 μM; 1 h) dose-dependently increases intracellular ADR accumulation in P-gp-overexpressing MCF-7/ADR human breast carcinoma cells[4]. 23-Hydroxybetulinic acid (0.2-20 μM; 1 h) dose-dependently increases intracellular VCR accumulation in P-gp-overexpressing MCF-7/ADR human breast carcinoma cells[4]. 23-hydroxybetulinic acid (6.25-100 μM; 6, 12, 24, 48 h) potently inhibits HL-60 cell proliferation in a dose- and time-dependent manner, with an IC50 of 20.12 μM at 48 h[5]. 23-hydroxybetulinic acid (12.5 μM; 24 h) induces formation of autophagic vacuoles in HL-60 cells[5]. 23-hydroxybetulinic acid (12.5-50 μM; 24 h) arrests HL-60 cells at the G1 phase of the cell cycle, with increasing G1 phase occupancy at higher concentrations[5]. 23-hydroxybetulinic acid (12.5-50 μM; 6, 12, 24 h) induces autophagic apoptosis in HL-60 cells in vitro in a time- and dose-dependent manner, with rates ranging from 11.60% to 78.73% across tested concentrations and times[5]. 23-hydroxybetulinic acid upregulates beclin-1mRNA expression in HL-60 cells in vitro in a dose-dependent manner[5]. 23-Hydroxybetulinic acid (0.2-20 μM; 24 h) concentration-dependently reduces Doxorubicin-induced cytotoxicity in rat H9c2 cells, increasing the IC50 of Doxorubicin to 12.94, 17.67, and 26.55 μM at concentrations of 0.2, 2, and 20 μM (for 24 h) respectively[6]. 23-Hydroxybetulinic acid (2.5-40 μM; 48 h) is non-toxic to THP-1-derived M0 macrophages at concentrations up to 20 μM after 48 h of incubation[7]. 23-Hydroxybetulinic acid (10-20 μM; 48 h) concentration-dependently inhibits IL-4-induced M2 polarization of THP-1-derived macrophages, as measured by reduced CD206 expression after 48 h of incubation[7]. 23-Hydroxybetulinic acid (10-20 μM; 48 h) concentration-dependently downregulates mRNA levels of M2-associated genes (CD206, Arg1, IL-10, CCL2) in IL-4-stimulated THP-1-derived macrophages after 48 h of incubation[7]. 23-Hydroxybetulinic acid (10-20 μM; 48 h) concentration-dependently inhibits IL-4-induced STAT6 phosphorylation and nuclear translocation in THP-1-derived macrophages after 48 h of incubation, via direct binding to STAT6[7]. 23-Hydroxybetulinic acid (20 μM; 48 h) inhibits IL-4-induced M2 polarization of THP-1-derived macrophages in a STAT6-dependent manner after 48 h of incubation with IL-4[7]. 23-Hydroxybetulinic acid (10-20 μM; 48 h) concentration-dependently inhibits IL-4-induced IL-10 secretion by THP-1-derived macrophages, as measured in conditioned medium after 72 h of serum-free culture following 48 h of 23-HBA incubation[7]. 23-Hydroxybetulinic acid (20 μM; 48 h) inhibits the IL-10/STAT3/Bcl-2 signaling pathway in 5-FU-treated SW480 colorectal cancer cells cultured in conditioned medium from 23-HBA-treated macrophages, after 48 h of 5-FU incubation[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
human chronic myelogenous leukemia K562 cells, mouse melanoma B16 cells, human cervical carcinoma HeLa cells, human umbilical vein endothelial HUVEC cells
Concentration:
0-300 μM
Incubation Time:
48 h
Result:
Inhibited proliferation of K562 cells with an IC50 of 39.9 μM, B16 cells with an IC50 of 78.5 μM, HeLa cells with an IC50 of 80.0 μM, and HUVEC cells with an IC50 of 94.8 μM. Caused decreased cell population and morphological shrinkage in K562 cells.
Increased the percentage of K562 cells in S phase from 26.35% (untreated) to 31.6%, 32.81%, and 52.34% at 20, 40, and 80 μM, respectively. Reduced G0/G1 and G2/M phase populations in a concentration-dependent manner.
Caused concentration-dependent increases in nuclear condensation (bright blue fluorescence) and uptake of PI (red fluorescence, indicating necrotic/advanced apoptotic cells) in K562 cells.\nIncreased total apoptotic K562 cells to 8.3%, 11.4%, and 18.2% at 20, 40, and 80 μM, respectively, compared to 3.8% in untreated cells.
Increased pro-apoptotic Bax, cytosolic cytochrome C, cleaved caspase-9, and cleaved caspase-3 levels in a concentration-dependent manner. Decreased anti-apoptotic Bcl-2 and survivin levels in a concentration-dependent manner.
Significantly inhibited viability of Huh-7, Hep3B, and Li-7 cells in a time- and concentration-dependent manner. Caused a more pronounced decline in cell viability at 20 μM for 72 h than for 48 h, with the strongest inhibitory effect observed in Huh-7 cells.
Caused dose-dependent nuclear shrinkage, cytoplasmic/nuclear fractionation, and formation of apoptotic bodies in Huh-7 cells, with increased numbers of apoptotic cells at higher concentrations.\nIncreased the apoptosis rate of Huh-7 cells in a concentration-dependent manner. Had its pro-apoptotic effect reversed by overexpression of Bcl-2.
Increased the IC50 of doxorubicin from 11.65 μM to 12.94, 17.67, and 26.55 μM respectively. Concentration-dependently improved the viability of doxorubicin-treated cells.
Concentration-dependently reduced IL-4-induced STAT6 phosphorylation with no effect on JAK2 phosphorylation. Inhibited nuclear translocation of p-STAT6. Bound to STAT6 with a docking score of -7.04, forming hydrogen bonds with Glu 219, Gln 281, and Pro 279 residues.
In Vivo
23-Hydroxybetulinic acid (10-20 mg/kg/day; daily; 4 weeks) dose-dependently suppresses hepatocellular carcinoma tumor growth, lung metastasis, and immunosuppression in nude mice, with 20 mg/kg producing near-complete elimination of lung metastases, while showing no obvious toxic effects[2]. 23-Hydroxybetulinic acid (20-100 mg/kg; i.g.; daily; 7 consecutive days; 1 hour prior to Doxorubicin (HY-15142) when in combination) alone has no significant in vivo antitumor activity in sarcoma 180-bearing mice, but when co-administered with doxorubicin, it produces synergistic antitumor effects (52% and 59% tumor weight reduction at 20 mg/kg and 100 mg/kg, respectively), increases intra-tumor doxorubicin accumulation, inhibits Doxorubicin-induced P-gp up-regulation, and alleviates Doxorubicin-induced cardiotoxicity[3]. 23-Hydroxybetulinic acid (20-80 mg/kg/day; i.g.; daily) dose-dependently alleviates Doxorubicin-induced cardiotoxicity in male Balb/c mice, with the 80 mg/kg/day oral dose reducing heart Doxorubicin accumulation by 46.52% and improving left ventricular ejection fraction to 75.68%[6]. 23-Hydroxybetulinic acid (7.5-15 mg/kg; i.p.; daily) inhibits M2 macrophage polarization via STAT6 signaling in mice, slightly reduces colorectal tumor weight alone, and enhances 5-Fluorouracil (5-FU) (HY-90006)'s anti-tumor efficacy by approximately 80% when co-administered, without causing obvious toxicity[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Reduced tumor volume and weight, with 20 mg/kg producing a more pronounced decline. Reduced positive expression of Ki-67, MMP2, and MMP9, and increased positive expression of cleaved caspase-3 in tumor tissues of mice treated with 20 mg/kg. Reduced the number of metastatic lung nodules in mice treated with 10 mg/kg, and eliminated almost all lung nodules in mice treated with 20 mg/kg. Reduced the percentage of CD11b+Gr1+ myeloid-derived suppressor cells (MDSCs) in a concentration-dependent manner. Caused no obvious body weight loss or pathological lesions in heart, liver, spleen, lung, or kidney tissues with either dose.
i.g.; daily; 7 consecutive days; 1 hour prior to Doxorubicin when in combination
Result:
Exerted no significant inhibitory effects on tumor weight when administered alone at 20 mg/kg or 100 mg/kg. Reduced tumor weight by 52% when co-administered with Doxorubicin at 20 mg/kg. Reduced tumor weight by 59% when co-administered with doxorubicin at 100 mg/kg; both combination groups showed significantly better therapeutic efficacy than Doxorubicin alone. Dose-dependently increased intra-tumor Doxorubicin concentration, with the 100 mg/kg dose producing a statistically significant increase. Had no effect on P-gp expression in tumors when administered alone. Significantly prevented doxorubicin-induced up-regulation of P-gp expression at 20 mg/kg and 100 mg/kg. Resulted in normal cardiac morphology when used in combination treatment, alleviating Doxorubicin-induced myocardial hemorrhagic spots. Caused no significant differences in mouse body weight across groups.
Slightly reduced tumor weight at 7.5 mg/kg or 15 mg/kg monotherapy. Reduced tumor weight by approximately 80% when co-administered with 5-FU at 15 mg/kg compared to the model group. Significantly reduced tumor weight when co-administered with 5-FU at 7.5 mg/kg compared to the model group. Did not cause significant changes in body weight, thymus index, or spleen index with monotherapy and co-treatment compared to relevant control groups. Significantly reduced the percentage of p-STAT6-positive area and CD206-positive area in tumor tissues at 7.5 mg/kg and 15 mg/kg compared to the model group. Induced significantly lower IL-10 mRNA levels and Bcl-2 expression in tumor tissues in the 15 mg/kg plus 5-FU group compared to the 5-FU monotherapy group.
DMSO : 100 mg/mL (211.55 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
2.1155 mL
10.5775 mL
21.1551 mL
5 mM
0.4231 mL
2.1155 mL
4.2310 mL
10 mM
0.2116 mL
1.0578 mL
2.1155 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.
Protocol 1
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (5.29 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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