Lupeol is a useful AR mold for developing new therapeutics to cure human elk cancer (CaP). After 48 hours of treatment, lupeol (10-50 μM) inhibited the proliferation of androtrophic phenotype (ADPC) cells, namely LAPC4 and LNCaP cells, with IC50 values of 15.9 and 17.3 μM. Lupeol reduced the development of 22Rv_1 with an IC50 of 19.1 μM. Lupeol inhibits C4-2b cell growth at an IC50 of 25 μM. Lupeol has the ability to inhibit ADPC and CRPC. Phenotypic CaP cell growth capacity. Androgens, through AR activation, are known to promote CaP cell proliferation [1].

One powerful medication that may reduce the tumorigenicity of CaP cells in the stroma is lupeol. Total circulatory PSA levels (via stromal tumor cell apoptosis) were assessed on day 56 of the research. At poststromal day 5 56, PSA levels in control rats with LNCaP and C4-2b tumors varied from 11.95 to 12.79 ng/mL, respectively. Conversely, rats treated with lopezol showed lower serum PSA levels, ranging from 4.25-7.09 ng/mL. Serum PSA levels were lower in tumor tissue from animals given lopeol than in control subjects [1].

Interactions
In in vivo studies using an orthotopic metastatic nude mouse oral and tongue squamous cell carcinoma model, 2 mg/mouse lupeol significantly reduced tumor volume and inhibited local metastasis, showing superior efficacy compared to cisplatin alone. Lupeol, when used in combination with low-dose cisplatin, exhibited significant synergistic cytotoxicity without side effects…
…This study…used an alkaline melting method to investigate the effect of lupeol on 7,12-dimethylbenzo[a]anthracene (DMBA)-induced DNA strand breaks in mouse skin. Samples were taken at 24, 48, 72, and 96 hours before or after a single topical application of DMBA (100 μg/mouse), and incremental doses of lupeol (50-200 μg/mouse) were administered topically. Both pretreatment and posttreatment with lupeol showed significant preventative effects against DMBA-induced DNA strand breaks (p<0.001), in a dose- and time-dependent manner. Pretreatment with 200 μg/mouse prevented 56.05% of DNA strand breaks after 96 hours; posttreatment prevented 43.26% of DNA strand breaks… This study evaluated the antigenotoxic effects of the triterpenoid compounds lupeol and mango pulp extract (MPE) in Swiss albino mice. The known mutagen benzo[a]pyrene (B[a]P) was administered intraperitoneally at a single dose of 100 mg/kg body weight. Seven days prior to B[a]P administration, mice were pretreated with lupeol (1 mg/mouse) and MPE (1 mL, 20%) via gavage. All animals were sacrificed at 24-hour sampling time, and chromosomal damage and micronucleus induction in their bone marrow tissue were analyzed. In the benzo[a]pyrene (B[a]P) treatment group, a significant increase in chromosomal aberrations and micronuclei, along with a decreased mitotic index, was observed. In the groups supplemented with lupeol or MPE, B[a]P-induced chromosome breakage was significantly reduced. Compared with the B[a]P-treated group, both lupeol and MPE reduced the incidence of abnormal cells and micronuclei. Furthermore, the anti-cytotoxic effects of lupeol or MPE were also significant, manifested by a significant increase in the mitotic index. Therefore, the results of this study indicate that lupeol and mango pulp extract (MPE) have a protective effect against benzo[a]pyrene (B[a]P)-induced chromosome breakage in Swiss albino mice. This study aimed to investigate the antioxidant effect of lupeol/mango pulp extract (MPE) on testosterone-induced oxidative stress in the prostate of male Swiss albino mice. …For 15 consecutive days, mice were orally administered lupeol (1 mg/mouse) and MPE (1 mL [20% w/v]/mouse), respectively, while simultaneously receiving a subcutaneous injection of testosterone (5 mg/kg body weight). At the end of the study, the prostate was dissected, and reactive oxygen species (ROS) levels, lipid peroxidation, and the activities of antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase, and glutathione S-transferase) were measured. Results: In testosterone-treated animals, increased ROS led to depletion of antioxidant enzymes and increased lipid peroxidation in the mouse prostate. However, lupeol/MPE treatment resulted in decreased ROS levels, and lipid peroxidation and antioxidant enzyme levels returned to normal. …These results indicate that lupeol/MPE effectively combats oxidative stress-induced prostate cell damage in mice…
For more complete interaction data (14 items in total) on lupeol, please visit the HSDB record page.

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Non-human toxicity values
Rats oral LD50 >2 g/kg /see table/
Mice oral LD50 >2 g/kg /see table/

[1]. Lupeol, a novel androgen receptor inhibitor: implications in prostate cancer therapy. Clin Cancer Res. 2011 Aug 15;17(16):5379-91.

Lupeol is a pentacyclic triterpenoid compound, a derivative of lupene, in which the hydrogen atom at the 3β position is replaced by a hydroxyl group. It is found in the seed coat of lupin seeds, as well as in the latex of fig and rubber trees. Additionally, it is present in many edible fruits and vegetables. It has anti-inflammatory properties and is a plant metabolite. Lupeol is a secondary alcohol belonging to the pentacyclic triterpenoid class. It is derived from the hydride of lupene. Lupeol has been studied for its use in treating acne. It has been reported to be found in tea (Camellia sinensis), holly leaf erythrorhiz (Acanthus ilicifolius), and other organisms with relevant data. See also: Calendula officinalis flower (part).

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Mechanism of Action
Lupinol is a triterpenoid compound found in fruits and vegetables. It selectively induces the death of large numbers of head and neck squamous cell carcinoma (HNSCC) cells, but has little effect on normal tongue fibroblast cell lines cultured in vitro. Downregulation of NF-κB is considered the main mechanism by which lupinol combats HNSCC. Lupinol not only inhibits tumor growth but also suppresses HNSCC cell invasion by reversing NF-κB-dependent epithelial-mesenchymal transition. Lupinol has a synergistic effect with cisplatin, enabling HNSCC cell lines with high NF-κB activity in vitro to become chemosensitized by cisplatin.

C30H50O

426.729

426.386

545-47-1

259846

White to off-white solid powder

1.0±0.1 g/cm3

488.1±14.0 °C at 760 mmHg

215-216ºC

216.9±12.4 °C

0.0±2.8 mmHg at 25°C

1.516

10.98

1

1

1

31

766

10

CC(=C)[C@@H]1CC[C@]2([C@H]1[C@H]3CC[C@@H]4[C@]5(CC[C@@H](C([C@@H]5CC[C@]4([C@@]3(CC2)C)C)(C)C)O)C)C

MQYXUWHLBZFQQO-QGTGJCAVSA-N

InChI=1S/C30H50O/c1-19(2)20-11-14-27(5)17-18-29(7)21(25(20)27)9-10-23-28(6)15-13-24(31)26(3,4)22(28)12-16-30(23,29)8/h20-25,31H,1,9-18H2,2-8H3/t20-,21+,22-,23+,24-,25+,27+,28-,29+,30+/m0/s1

Lup-20(29)-en-3-ol, (3-beta)-

NSC 90487Monogynol BLupeol β-ViscolClerodol Fagarasterol Lupenol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Ethanol : ~14.29 mg/mL (~33.49 mM)
DMSO : ~2 mg/mL (~4.69 mM)

Solubility in Formulation 1: ≥ 1.43 mg/mL (3.35 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 14.3 mg/mL clear EtOH + stock solution to 900 μL of corn oil and mix well.

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Solubility in Formulation 2: 20 mg/mL (46.87 mM) in Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)