23-Hydroxybetulinic acid (Synonyms: 23-羟基白桦酸; Anemosapogenin)

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23-Hydroxybetulinic acid (Anemosapogenin) 是一种具有口服活性的具有广谱抗癌活性的三萜类化合物。23-Hydroxybetulinic acid 可降低 Bcl-2 和 survivin 水平，升高 Bax 水平，促进 caspase-3 和 caspase-9 的剪切/活化，并通过包括细胞色素 C 释放和线粒体膜电位破坏在内的内源性线粒体通路诱导细胞凋亡 (apoptosis)。23-Hydroxybetulinic acid 可将细胞周期阻滞于 S 和 G1 期，抑制癌细胞增殖，阻断 MAPK 信号通路，调控 MMP2，并通过上调 beclin-1 诱导自噬性凋亡。23-Hydroxybetulinic acid 可抑制 P-gp 的活性和外排功能，增加细胞内化疗药物的蓄积量，并与 Doxorubicin (HY-15142) 协同增强细胞毒性。23-Hydroxybetulinic acid 可抑制 STAT6 的磷酸化和核转位，阻断 M2 型巨噬细胞极化，降低 M2 型巨噬细胞介导的结肠癌细胞凋亡抵抗。23-Hydroxybetulinic acid 可用于慢性髓系白血病、肝细胞癌、肉瘤 180 癌、多药耐药乳腺癌、Doxorubicin 诱导的心脏毒性以及结直肠癌的相关研究。

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23-Hydroxybetulinic acid Chemical Structure

CAS No. : 85999-40-2

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规格	价格	是否有货
10 mM * 1 mL in DMSO	￥510	In-stock
1 mg	￥215	In-stock
5 mg	￥490	In-stock
10 mg	￥722	In-stock
25 mg	￥1444	In-stock
50 mg	￥2166	In-stock
100 mg	￥3250	In-stock
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Other Forms of 23-Hydroxybetulinic acid:

23-Hydroxybetulinic acid (Standard) 询价

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生物活性
纯度 & 产品资料
参考文献

生物活性

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].

IC₅₀ & Target^[1]^[2]

Caspase 3

Caspase-9

Bax

Bcl-2

MMP-2

细胞效力
(Cellular Effect)

Cell Line	Type	Value	Description	References
A-375	IC₅₀	41.99 μM Compound: 1	Antiproliferative activity against human A375 cells after 72 hrs by MTT assay Antiproliferative activity against human A375 cells after 72 hrs by MTT assay	[PMID: 21496972]
A-375	IC₅₀	76.3 μM Compound: 1; HBA	Antiproliferative activity against human A375 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human A375 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31491611]
A2780	IC₅₀	79.12 μM Compound: 1; HBA	Antiproliferative activity against human A2780 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human A2780 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31491611]
A549	IC₅₀	51.44 μM Compound: 23-HBA; 4	Antiproliferative activity against human A549 cells overexpressing NQO1 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Antiproliferative activity against human A549 cells overexpressing NQO1 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 35803175]
A549	IC₅₀	87.6 μM Compound: HBA	Cytotoxicity against human A549 cells by MTT assay Cytotoxicity against human A549 cells by MTT assay	[PMID: 17275295]
B16	IC₅₀	18.68 μM Compound: 1	Antiproliferative activity against mouse B16 cells after 72 hrs by MTT assay Antiproliferative activity against mouse B16 cells after 72 hrs by MTT assay	[PMID: 21496972]
B16	IC₅₀	29.87 μM Compound: 1, HBA	Antiproliferative activity against mouse B16 cells after 72 hrs by MTT assay Antiproliferative activity against mouse B16 cells after 72 hrs by MTT assay	[PMID: 25529742]
B16	IC₅₀	29.87 μM Compound: 1, HBA	Antiproliferative activity against mouse B16 cells assessed as growth inhibition after 72 hrs by MTT assay Antiproliferative activity against mouse B16 cells assessed as growth inhibition after 72 hrs by MTT assay	[PMID: 25984840]
B16	IC₅₀	29.87 μM Compound: HBA	Antiproliferative activity against mouse B16 cells after 72 hrs MTT assay Antiproliferative activity against mouse B16 cells after 72 hrs MTT assay	[PMID: 25247772]
B16	IC₅₀	83.04 μM Compound: HBA	Cytotoxicity against mouse B16 cells by MTT assay Cytotoxicity against mouse B16 cells by MTT assay	[PMID: 17275295]
B16-F10	IC₅₀	24.46 μM Compound: 1; 23-HBA	Antiproliferative activity against mouse B16F10 cells after 72 hrs by MTT assay Antiproliferative activity against mouse B16F10 cells after 72 hrs by MTT assay	[PMID: 30344912]
Bel-7402	IC₅₀	39.67 μM Compound: 1, HBA	Antiproliferative activity against human Bel7402 cells after 72 hrs by MTT assay Antiproliferative activity against human Bel7402 cells after 72 hrs by MTT assay	[PMID: 25529742]
Bel-7402	IC₅₀	39.67 μM Compound: 1, HBA	Antiproliferative activity against human Bel7402 cells assessed as growth inhibition after 72 hrs by MTT assay Antiproliferative activity against human Bel7402 cells assessed as growth inhibition after 72 hrs by MTT assay	[PMID: 25984840]
Bel-7402	IC₅₀	39.67 μM Compound: HBA	Antiproliferative activity against human Bel7402 cells after 72 hrs MTT assay Antiproliferative activity against human Bel7402 cells after 72 hrs MTT assay	[PMID: 25247772]
Bel-7402	IC₅₀	97.32 μM Compound: HBA	Cytotoxicity against human BEL-7402 cells by MTT assay Cytotoxicity against human BEL-7402 cells by MTT assay	[PMID: 17275295]
C6	IC₅₀	99.48 μM Compound: HBA	Cytotoxicity against mouse C6 cells by MTT assay Cytotoxicity against mouse C6 cells by MTT assay	[PMID: 17275295]
HFL1	IC₅₀	75 μM Compound: 23-HBA; 4	Cytotoxicity against human HFL1 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Cytotoxicity against human HFL1 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 35803175]
HL-60	IC₅₀	45.15 μM Compound: 1, HBA	Antiproliferative activity against human HL60 cells after 72 hrs by MTT assay Antiproliferative activity against human HL60 cells after 72 hrs by MTT assay	[PMID: 25529742]
HL-60	IC₅₀	45.15 μM Compound: 1, HBA	Antiproliferative activity against human HL60 cells assessed as growth inhibition after 72 hrs by MTT assay Antiproliferative activity against human HL60 cells assessed as growth inhibition after 72 hrs by MTT assay	[PMID: 25984840]
HL-60	IC₅₀	45.15 μM Compound: HBA	Antiproliferative activity against human HL60 cells after 72 hrs MTT assay Antiproliferative activity against human HL60 cells after 72 hrs MTT assay	[PMID: 25247772]
HT-29	IC₅₀	54.81 μM Compound: 23-HBA; 4	Antiproliferative activity against human HT-29 cells overexpressing NQO1 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Antiproliferative activity against human HT-29 cells overexpressing NQO1 assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 35803175]
HeLa	IC₅₀	46.22 μM Compound: 1	Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay	[PMID: 21496972]
HeLa	IC₅₀	52.39 μM Compound: 1, HBA	Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay	[PMID: 25529742]
HeLa	IC₅₀	52.39 μM Compound: 1, HBA	Antiproliferative activity against human HeLa cells assessed as growth inhibition after 72 hrs by MTT assay Antiproliferative activity against human HeLa cells assessed as growth inhibition after 72 hrs by MTT assay	[PMID: 25984840]
HeLa	IC₅₀	52.39 μM Compound: HBA	Antiproliferative activity against human HeLa cells after 72 hrs MTT assay Antiproliferative activity against human HeLa cells after 72 hrs MTT assay	[PMID: 25247772]
HepG2	IC₅₀	41.41 μM Compound: 1	Antiproliferative activity against human HepG2 cells after 72 hrs by MTT assay Antiproliferative activity against human HepG2 cells after 72 hrs by MTT assay	[PMID: 21496972]
HepG2	IC₅₀	71.84 μM Compound: 1; HBA	Antiproliferative activity against human HepG2 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human HepG2 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31491611]
L02	IC₅₀	79.15 μM Compound: 1; HBA	Cytotoxicity against human L02 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay Cytotoxicity against human L02 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31491611]
M14	IC₅₀	50 μM Compound: 7	Cytotoxicity against human M14 cells after 48 hrs by MTT assay Cytotoxicity against human M14 cells after 48 hrs by MTT assay	[PMID: 21954959]
MCF7	IC₅₀	20.83 μM Compound: 1; 23-HBA	Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay	[PMID: 30344912]
MCF7	IC₅₀	46.61 μM Compound: 1	Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay	[PMID: 21496972]
MCF7	IC₅₀	74.98 μM Compound: 1; HBA	Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay	[PMID: 31491611]
NCI-H596	IC₅₀	58.12 μM Compound: 23-HBA; 4	Antiproliferative activity against NQO1-deficient human NCI-H596 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Antiproliferative activity against NQO1-deficient human NCI-H596 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 35803175]

体外研究
(In Vitro)

23-Hydroxybetulinic acid (0-300 μM; 48 h) 可强效抑制人慢性粒细胞白血病 K562 细胞的增殖 (IC₅₀ = 39.9 μM)，且对 B16、HeLa 和 HUVEC 细胞的细胞毒性较低^[1]。
23-Hydroxybetulinic acid (0-80 μM; 24 h) 可在处理 24 h 后诱导人慢性粒细胞白血病 K562 细胞发生浓度依赖性的 S 期细胞周期阻滞，其中 80 μM HBA 可将 S 期细胞比例提升至 52.34%^[1]。
23-Hydroxybetulinic acid (20-80 μM; 24 h) 经 Hoechst33342/PI 双染色检测显示，处理 24 h 后可在人慢性粒细胞白血病 K562 细胞中诱导浓度依赖性凋亡^[1]。
23-Hydroxybetulinic acid (20-80 μM; 24 h) 可显著破坏人慢性粒细胞白血病 K562 细胞的线粒体膜电位，经 24 h 处理后，80 μM HBA 可将红/绿荧光比率降至 0.38^[1]。
23-Hydroxybetulinic acid (10-80 μM; 24 h) 可在作用 24 小时后诱导人慢性粒细胞白血病 K562 细胞激活内源性 (线粒体) 凋亡通路，其机制为通过浓度依赖性方式调控促凋亡与抗凋亡蛋白，并激活胱天蛋白酶^[1]。
23-Hydroxybetulinic acid (1.25-20 μM; 48-72 h) 可呈时间和浓度依赖性抑制 Huh-7、Hep3B 和 Li-7 人肝癌细胞的活力，其中以 20 μM 作用 72 h 时对 Huh-7 细胞的抑制效果最强^[2]。
23-Hydroxybetulinic acid (1.25-20 μM; 2-3 weeks) 可在 2-3 周内抑制人肝癌细胞 Huh-7、Hep3B 和 Li-7 的集落形成，其中对 Huh-7 细胞的作用效果最强^[2]。
23-Hydroxybetulinic acid (5-20 μM; 48 h) 可呈浓度依赖性诱导人肝癌 Huh-7 细胞凋亡，且该效应可被 Bcl-2 过表达逆转^[2]。
23-Hydroxybetulinic acid (5-20 μM) 可调控人肝癌 Huh-7 细胞中凋亡相关蛋白的表达，以浓度依赖的方式上调 Bax，并下调 Bcl-2 与活化型 caspase-3^[2]。
23-Hydroxybetulinic acid (5-20 μM) 可调控人肝癌 Huh-7 细胞的迁移/侵袭以及 MAPK 通路相关蛋白的表达，以浓度依赖的方式降低 MMP2、MMP9、p-MEK1/2 和 p-ERK1/2 的水平，同时上调 TIMP2 的表达^[2]。
23-Hydroxybetulinic acid (5-20 μM; 48 h) 可呈浓度依赖性抑制人肝癌 Huh-7 细胞的迁移和侵袭能力^[2]。
23-Hydroxybetulinic acid (48 h) 可剂量依赖性地抑制 NCI-H460、SGC7901、HepG2 及肉瘤 180 细胞的生长，其平均 IC₅₀ 值分别为 49.2 μM、49.1 μM、306.4 μM 和 28.0 μM^[3]。
23-Hydroxybetulinic acid (0.2-20 μM; 48 h) 可呈剂量依赖性地增强 Driamaycin 对过表达 P-gp 的人乳腺癌细胞 MCF-7/ADR 的细胞毒性，降低细胞存活率^[4]。
23-Hydroxybetulinic acid (0.2-20 μM; 48 h) 可呈剂量依赖性地增强 VCR 对过表达 P-gp 的人乳腺癌细胞 MCF-7/ADR 的细胞毒性，降低细胞存活率^[4]。
23-Hydroxybetulinic acid (2-20 μM) 可呈剂量依赖性地增强 ADR 诱导的过表达 P-糖蛋白 (P-gp) 的人乳腺癌细胞 MCF-7/ADR 的凋亡^[4]。
23-Hydroxybetulinic acid (0.2-20 μM; 1 h) 可剂量依赖性地增加过表达 P-gp 的人乳腺癌 MCF-7/ADR 细胞内的 ADR 蓄积^[4]。
23-Hydroxybetulinic acid (0.2-20 μM; 1 h) 可剂量依赖性地增加过表达 P-gp 的人乳腺癌细胞 MCF-7/ADR 中的细胞内 VCR 蓄积^[4]。
23-hydroxybetulinic acid (6.25-100 μM; 6, 12, 24, 48 h) 可呈剂量和时间依赖性强效抑制 HL-60 细胞增殖，在 48 h 时的 IC₅₀ 为 20.12 μM^[5]。
23-hydroxybetulinic acid (12.5 μM; 24 h) 可诱导 HL-60 细胞中自噬小泡的形成^[5]。
23-hydroxybetulinic acid (12.5-50 μM; 24 h) 可将 HL-60 细胞阻滞于细胞周期的 G1 期，且随着浓度升高，G1 期细胞占比增加^[5]。
23-hydroxybetulinic acid (12.5-50 μM; 6, 12, 24 h) 可在体外以时间和剂量依赖的方式诱导 HL-60 细胞发生自噬性凋亡，在测试的浓度和时间范围内，其凋亡率为 11.60% 至 78.73%^[5]。
23-hydroxybetulinic acid 可在体外以剂量依赖方式上调 HL-60 细胞中 beclin-1 的 mRNA 表达水平^[5]。
23-Hydroxybetulinic acid (0.2-20 μM; 24 h) 可浓度依赖性地减轻 Doxorubicin 对大鼠 H9c2 细胞的细胞毒性，在 0.2、2 和 20 μM (for 24 h) 的浓度下，分别将 Doxorubicin 的 IC₅₀ 提升至 12.94、17.67 和 26.55 μM^[6]。
23-Hydroxybetulinic acid (2.5-40 μM; 48 h) 在孵育 48 h 后，浓度高达 20 μM 时对 THP-1 来源的 M0 巨噬细胞无毒性^[7]。
23-Hydroxybetulinic acid (10-20 μM; 48 h) 可浓度依赖性地抑制 IL-4 诱导的 THP-1 来源巨噬细胞向 M2 型极化，该作用通过孵育 48 h 后 CD206 表达水平降低得到验证^[7]。
23-Hydroxybetulinic acid (10-20 μM; 48 h) 可浓度依赖性地下调经 IL-4 刺激的 THP-1 来源巨噬细胞中 M2 相关基因 (CD206、Arg1、IL-10、CCL2) 的 mRNA 水平，孵育时长为 48 h^[7]。
23-Hydroxybetulinic acid (10-20 μM; 48 h) 呈浓度依赖性抑制 IL-4 诱导的 THP-1 来源巨噬细胞中 STAT6 的磷酸化与核转位，其作用机制为直接结合 STAT6^[7]。
23-Hydroxybetulinic acid (20 μM; 48 h) 以依赖 STAT6 的方式抑制 IL-4 诱导的 THP-1 来源巨噬细胞向 M2 型极化，该实验在与 IL-4 共同孵育 48 h 后开展^[7]。
23-Hydroxybetulinic acid (10-20 μM; 48 h) 可浓度依赖性地抑制 THP-1 来源巨噬细胞中由 IL-4 诱导的 IL-10 分泌；该检测是在 23-HBA 孵育 48 h 后，经无血清培养 72 h 的条件培养基中完成的^[7]。
23-Hydroxybetulinic acid (20 μM; 48 h) 可抑制经 23-HBA 处理的巨噬细胞条件培养基中培养、且经 5-FU 孵育 48 h 的 SW480 结直肠癌细胞中的 IL-10/STAT3/Bcl-2 信号通路^[7]。

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

Cell Cytotoxicity Assay^[1]

Cell Line:	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.

Cell Cycle Analysis^[1]

Cell Line:	human chronic myelogenous leukemia K562 cells
Concentration:	20 μM; 40 μM; 80 μM
Incubation Time:	24 h
Result:	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.

Apoptosis Analysis^[1]

Cell Line:	human chronic myelogenous leukemia K562 cells
Concentration:	20 μM; 40 μM; 80 μM
Incubation Time:	24 h
Result:	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.

Western Blot Analysis^[1]

Cell Line:	human chronic myelogenous leukemia K562 cells
Concentration:	10 μM; 20 μM; 40 μM; 80 μM
Incubation Time:	24 h
Result:	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.

Cell Viability Assay^[2]

Cell Line:	Huh-7, Hep3B, Li-7 (human hepatocellular carcinoma cell lines)
Concentration:	1.25 μM; 2.5 μM; 5 μM; 10 μM; 20 μM
Incubation Time:	48 h; 72 h
Result:	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.

Apoptosis Analysis^[2]

Cell Line:	Huh-7 (human hepatocellular carcinoma cell line)
Concentration:	5 μM; 10 μM; 20 μM
Incubation Time:	48 h
Result:	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.

Cell Migration Assay ^[2]

Cell Line:	Huh-7 (human hepatocellular carcinoma cell line)
Concentration:	5 μM; 10 μM; 20 μM
Incubation Time:	48 h
Result:	Inhibited migration of Huh-7 cells in a concentration-dependent manner, with more pronounced inhibition at higher concentrations.

Cell Invasion Assay^[2]

Cell Line:	Huh-7 (human hepatocellular carcinoma cell line)
Concentration:	5 μM; 10 μM; 20 μM
Incubation Time:	48 h
Result:	Inhibited invasion of Huh-7 cells in a concentration-dependent manner, with more pronounced inhibition at higher concentrations.

Cell Autophagy Assay^[5]

Cell Line:	HL-60
Concentration:	12.5 μM
Incubation Time:	24 h
Result:	Induced formation of numerous autophagic vacuoles and empty vacuoles in treated cells.

Apoptosis Analysis^[5]

Cell Line:	HL-60
Concentration:	12.5-50 μM
Incubation Time:	6, 12, 24 h
Result:	Induced autophagic apoptosis with rates of 11.60% (12.5 μM, 6 h), 17.49% (12.5 μM, 12 h), 28.37% (12.5 μM, 24 h), 25.90% (25 μM, 6 h), 49.00% (25 μM, 12 h), 72.20% (25 μM, 24 h), 28.17% (50 μM, 6 h), 60.69% (50 μM, 12 h), 78.73% (50 μM, 24 h).

Cell Viability Assay^[6]

Cell Line:	rat H9c2 cells
Concentration:	0.2, 2, 20 μM
Incubation Time:	24 h
Result:	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.

RT-PCR^[7]

Cell Line:	THP-1-derived macrophages
Concentration:	10-20 μM (co-incubated with IL-4)
Incubation Time:	48 h
Result:	Concentration-dependently reduced the IL-4-induced upregulation of CD206, Arg1, IL-10, and CCL2 mRNA levels.

Western Blot Analysis^[7]

Cell Line:	THP-1-derived macrophages
Concentration:	10-20 μM (co-incubated with IL-4)
Incubation Time:	48 h
Result:	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.

体内研究
(In Vivo)

23-Hydroxybetulinic acid (10-20 mg/kg/天；每日给药；持续 4 周) 可在裸鼠中呈剂量依赖性地抑制肝细胞癌的肿瘤生长、肺转移及免疫抑制，其中 20 mg/kg 剂量可实现肺转移的近乎完全清除，且未表现出明显的毒性作用^[2]。
23-Hydroxybetulinic acid (20-100 mg/kg；灌胃；每日一次；连续 7 天；联合给药时于 Doxorubicin (HY-15142) 给药前 1 小时给予) 单独使用对荷肉瘤 180 小鼠无显著体内抗肿瘤活性，但与 Doxorubicin 联用时可产生协同抗肿瘤效应 (20 mg/kg 和 100 mg/kg 剂量下分别使肿瘤重量降低 52%和 59%)，增加肿瘤内 Doxorubicin 的蓄积量，抑制 Doxorubicin 诱导的 P-gp 上调，并缓解 Doxorubicin 诱导的心脏毒性^[3]。
23-Hydroxybetulinic acid (20-80 mg/kg/day；灌胃；每日) 可剂量依赖性地缓解 Doxorubicin 诱导的雄性 Balb/c 小鼠心脏毒性，其中 80 mg/kg/day 口服剂量可使心脏中 Doxorubicin 的蓄积量降低 46.52%，并将左心室射血分数改善至 75.68%^[6]。
23-Hydroxybetulinic acid (7.5-15 mg/kg；腹腔注射；每日一次) 可在小鼠中通过 STAT6 信号通路抑制 M2 型巨噬细胞极化，单独使用时可轻度降低结直肠癌肿瘤重量，与 5-Fluorouracil (5-FU) (HY-90006) 联用时可将其抗肿瘤疗效提升约 80%，且无明显毒性^[7]。

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

Animal Model:	BALB/c nude mice (male, 4-6 weeks old, 18-20 g, subcutaneously injected with HCC cells)^[2]
Dosage:	10 mg/kg/day; 20 mg/kg/day
Administration:	daily; 4 weeks
Result:	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.

Animal Model:	ICR (male, 18-22 g)^[3]
Dosage:	20 mg/kg; 100 mg/kg
Administration:	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.

Animal Model:	BALB/c (male, 6-8 weeks old, 20±2 g, subcutaneous injection of 2×10⁶ CT26 cells)^[7]
Dosage:	7.5 mg/kg; 15 mg/kg
Administration:	i.p. (daily); i.p. (once every 3 days, 5-FU)
Result:	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.

分子量

472.70

Formula

C₃₀H₄₈O₄

CAS 号

85999-40-2

性状

固体

颜色

White to off-white

中文名称

23-羟基白桦酸；23-羟基白桦脂酸

结构分类

初始来源

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

-20°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

溶解性数据

细胞实验：

DMSO 中的溶解度 : 100 mg/mL (211.55 mM; 超声助溶; 吸湿的 DMSO 对产品的溶解度有显著影响，请使用新开封的 DMSO)

配制储备液

浓度溶剂体积质量	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

查看完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。

摩尔计算器
稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

This equation is commonly abbreviated as: C₁V₁ = C₂V₂

浓度 _(start)

体积 _(start)

浓度 _(final)

体积 _(final)

动物实验：

请根据您的实验动物和给药方式选择适当的溶解方案。

以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用；
以下溶剂前显示的百分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

方案一

请依序添加每种溶剂： 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (5.29 mM); 澄清溶液

此方案可获得 ≥ 2.5 mg/mL（饱和度未知）的澄清溶液，此方案实验周期在半个月以上的动物实验酌情使用。
以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

动物溶解方案计算器

请输入动物实验的基本信息：

给药剂量

mg/kg

动物的平均体重

每只动物的给药体积

μL

动物数量

只

由于实验过程有损耗，建议您多配一只动物的量

请输入您的动物体内配方组成：

DMSO +

Tween-80 +

Saline

如果您的动物是免疫缺陷鼠或者体弱鼠，建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。

方案所需 助溶剂 包括：DMSO，，均可在 MCE 网站选购。，Tween 80，均可在 MCE 网站选购。

计算结果

工作液所需浓度 : mg/mL

储备液配制方法 : mg 药物溶于 μL DMSO（母液浓度为 mg/mL）。

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

您所需的储备液浓度超过该产品的实测溶解度，以下方案仅供参考，如有需要，请与 MCE 中国技术支持联系。

动物实验体内工作液的配制方法 : 取 μL DMSO 储备液，加入 μL 。 μL ，混合均匀至澄清，再加 μL Tween 80，混合均匀至澄清，再加 μL 生理盐水。

连续给药周期超过半月以上，请谨慎选择该方案。

请确保第一步储备液溶解至澄清状态，从左到右依次添加助溶剂。您可采用超声加热（超声清洗仪，建议频次 20-40 kHz），涡旋吹打等方式辅助溶解。

纯度 & 产品资料

纯度: 99.44%

选择批次：

Data Sheet (701 KB) SDS (254 KB)

COA (272 KB) HNMR (203 KB) CNMR (179 KB) RP-HPLC (257 KB) MS (184 KB)

产品使用指南 (1538 KB)

参考文献

[1]. Liu M, et al. Cytotoxicity of the compounds isolated from Pulsatilla chinensis saponins and apoptosis induced by 23-hydroxybetulinic acid. Pharm Biol. 2015;53(1):1-9. [Content Brief]

[2]. Tian D, et al. 23-hydroxybetulinic acid reduces tumorigenesis, metastasis and immunosuppression in a mouse model of hepatocellular carcinoma via disruption of the MAPK signaling pathway. Anticancer Drugs. 2022;33(9):815-825. [Content Brief]

[3]. Zheng Y, et al. 23-Hydroxybetulinic acid from Pulsatilla chinensis (Bunge) Regel synergizes the antitumor activities of doxorubicin in vitro and in vivo. J Ethnopharmacol. 2010;128(3):615-622. [Content Brief]

[4]. Liu Z, et al. Involvement of P-gp on Reversing Multidrug Resistance Effects of 23-Hydroxybetulinic Acid on Chemotherapeutic Agents. Front Pharmacol. 2021 Dec 15;12:796745. [Content Brief]

[5]. Ye B, et al. 23-hydroxybetulinic acid-induced HL-60 cell autophagic apoptosis and its molecular mechanism. Nat Prod Res. 2012;26(11):1063-8. [Content Brief]

[6]. Zhou F, et al. Protective effect of 23-hydroxybetulinic acid on doxorubicin-induced cardiotoxicity: a correlation with the inhibition of carbonyl reductase-mediated metabolism. Br J Pharmacol. 2015;172(23):5690-5703. [Content Brief]

[7]. Fan Z, et al. 23-Hydroxybetulinic acid attenuates 5-fluorouracil resistance of colorectal cancer by modulating M2 macrophage polarization via STAT6 signaling. Cancer Immunol Immunother. 2024;73(5):83. Published 2024 Mar 30. [Content Brief]

23-Hydroxybetulinic acid 相关分类

完整储备液配制表

可选溶剂	浓度溶剂体积质量	1 mg	5 mg	10 mg	25 mg

DMSO	1 mM	2.1155 mL	10.5775 mL	21.1551 mL	52.8877 mL
	5 mM	0.4231 mL	2.1155 mL	4.2310 mL	10.5775 mL
	10 mM	0.2116 mL	1.0578 mL	2.1155 mL	5.2888 mL
	15 mM	0.1410 mL	0.7052 mL	1.4103 mL	3.5258 mL
	20 mM	0.1058 mL	0.5289 mL	1.0578 mL	2.6444 mL
	25 mM	0.0846 mL	0.4231 mL	0.8462 mL	2.1155 mL
	30 mM	0.0705 mL	0.3526 mL	0.7052 mL	1.7629 mL
	40 mM	0.0529 mL	0.2644 mL	0.5289 mL	1.3222 mL
	50 mM	0.0423 mL	0.2116 mL	0.4231 mL	1.0578 mL
	60 mM	0.0353 mL	0.1763 mL	0.3526 mL	0.8815 mL
	80 mM	0.0264 mL	0.1322 mL	0.2644 mL	0.6611 mL
	100 mM	0.0212 mL	0.1058 mL	0.2116 mL	0.5289 mL

Help & FAQs

Do most proteins show cross-species activity?
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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23-Hydroxybetulinic acid (Synonyms: 23-羟基白桦酸; Anemosapogenin)

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23-Hydroxybetulinic acid (Synonyms: 23-羟基白桦酸; Anemosapogenin)

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