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Bavachinin (BVC; 7-O-Methylbavachin; Bavachinin A)

Alias: 7-O-Methylbavachin; Bavachinin; 19879-30-2; Bavachinin A; 7-O-Methylbavachin; 4H-1-Benzopyran-4-one, 2,3-dihydro-2-(4-hydroxyphenyl)-7-methoxy-6-(3-methyl-2-buten-1-yl)-, (2S)-; VL3EV483SZ; UNII-VL3EV483SZ; BRN 3629340;
Cat No.:V4468 Purity: ≥98%
Bavachinin(BVC; 7-O-Methylbavachin; Bavachinin A) is a naturally occuring compound isolated from the fruit of the traditional Chinese herb Fructus Psoraleae (FP).
Bavachinin (BVC; 7-O-Methylbavachin; Bavachinin A)
Bavachinin (BVC; 7-O-Methylbavachin; Bavachinin A) Chemical Structure CAS No.: 19879-30-2
Product category: Beta Amyloid
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Bavachinin (BVC; 7-O-Methylbavachin; Bavachinin A) is a naturally occuring compound isolated from the fruit of the traditional Chinese herb Fructus Psoraleae (FP). It has potent anti-angiogenic activity.

Biological Activity I Assay Protocols (From Reference)
Targets
PPAR-γ(IC50 = 0.622 μM); PPARα (IC50 = 21.043 μM); PPARδ (IC50 = 12.819 μM); HIF-1α
ln Vitro
This study aimed to demonstrate that the natural compound, Bavachinin, has potent anti-angiogenic activity in vitro and in vivo. Bavachinin inhibited increases in HIF-1α activity in human KB carcinoma (HeLa cell derivative) and human HOS osteosarcoma cells under hypoxia in a concentration-dependent manner, probably by enhancing the interaction between von Hippel-Lindau (VHL) and HIF-1α. Furthermore, Bavachinin decreased transcription of genes associated with angiogenesis and energy metabolism that are regulated by HIF-1, such as vascular endothelial growth factors (VEGF), Glut 1 and Hexokinase 2. Bavachinin also inhibited tube formation in human umbilical vein endothelial cells (HUVECs) as well as in vitro migration of KB cells. [2]
Bavachinin inhibits Th2 cell differentiation [3]
To investigate the effect of Bavachinin on Th2 cell differentiation, splenocytes from IL-4-GFP (4get) mice were activated with concanavalin A in the presence of IL-4 for 48 h, and the percentage of GFP+ cells was analyzed by flow cytometry. We observed that Bavachinin significantly reduced the percentage of GFP+ cells in a dose-dependent manner (Figure 1a and b). This reduction reflected the inhibition of IL-4 expression, as analyzed by quantitative PCR. Similarly, Bavachinin inhibited the mRNA expression of both IL-5 and IL-13 (Figure 1c). These results indicate that Bavachinin inhibits Th2 cell cytokine expression.
Bavachinin (BNN), one of the main active ingredients of Psoraleacorylifolia, can activate peroxisome proliferator-activated receptor γ (PPARγ). PPARγ has become a promising therapeutic target in cancer. The aim of the present study was to explore the antitumor effects of BNN in non-small cell lung cancer (NSCLC). Cell Counting Kit-8 and lactate dehydrogenase release assays were performed to measure cell toxicity. Western blotting and immunofluorescence were used to analyze the expression of apoptosis-related factors and PPARγ. The ability of PPARγ to bind to BNN was evaluated by drug affinity responsive target stability (DARTS) and cellular thermal shift assay (CETSA). A reactive oxygen species (ROS) assay kit was used to detect the ROS level. The results revealed that the survival rates and cell viability of A549 cells were reduced by BNN in a dose-dependent manner. The present results also demonstrated that BNN dose-dependently changed the expression of Bcl-2, Bax, caspases-3/9 and PPARγ. In addition, through the cytotoxic and anti-proliferative effects, the apoptosis-related proteins' inhibitive properties of BNN were completely inhibited by the PPARγ antagonists T0070907 and GW9662. The DARTS and CETSA results confirmed the protein binding activity of PPARγ. Furthermore, it was demonstrated that the BNN-induced ROS generation was dependent on PPARγ activation. Taken together, the present study demonstrated that BNN induced the death of A549 cells by activating PPARγ, an effect mediated by the increased ROS level. These results highlighted the potential role of BNN as a chemotherapeutic agent against NSCLC.[4]
BVC/Bavachinin is a natural pan-PPAR agonist with potent binding affinities [5]
A reporter gene assay was used to determine the activities of BVC/Bavachinin on PPAR-α, -β/δ or -γ. As shown in Fig. 1, BVC (Fig. 1a) dose-dependently induced the transcriptional activities of the mouse LBD (Fig. 1b–d) and full lengths (Fig. 1e−g) of the three PPAR isoforms. Notably, BVC showed stronger activities with PPAR-γ than with PPAR-α and PPAR-β/δ (EC50 = 0.74 μmol/l, 4.00 μmol/l and 8.07 μmol/l, respectively; Table 1). To examine the cellular effect of BVC on PPAR-γ, insulin, dexamethasone and RSG or BVC were used to induce differentiation of 3T3-L1 pre-adipocytes. BVC promoted 3T3-L1 adipocyte differentiation in a dose-dependent manner (Fig. 1h). 3T3-L1 differentiation was effectively activated by 1 μmol/l BVC, and almost fully by 10 μmol/l BVC. The results suggest that BVC activates PPAR-γ at a cellular level.

Competitive binding assays (Fig. 1i–k) showed that BVC/Bavachinin had stronger binding to human PPAR-γ (K i = 223 nmol/l; Table 1) than to human PPAR-α and -β/δ (K i = 7.88 and 5.28 μmol/l; Table 1). Moreover, BVC has a fivefold weaker binding affinity than RSG for PPAR-γ, and has twofold stronger binding affinity than fenofibric acid and WY14643 for PPAR-α.

In contrast to the full PPAR-γ agonist RSG and PPAR-α agonist GW7647, BVC/Bavachinin did not induce the recruitment of classic transcriptional cofactors, peroxisome proliferative activated receptor, gamma, coactivator 1 α (PGC1α) and mediator complex subunit 1 (TRAP220/DRIP) (ESM Fig. 1a–c). Using reporter gene and coactivator recruitment assays, BVC did not activate other nuclear receptors related to the metabolic syndrome, such as liver x receptor (LXR)-α, LXR-β/δ and farnesoid x receptor (FXR) (ESM Fig. 1d–g), suggesting the specificity of BVC for PPARs.
ln Vivo
In nude mice, babachinin (5 mg/kg; intraperitoneal injection; seven consecutive days) can impede kit KB tumor growth and angiogenesis [2]. Tumors in mice can be treated with bevacidin (50 mg/kg; intraperitoneal injection; seven consecutive days).
Bavachinin reduced tumor growth and microvessel formation [2]
In order to confirm that Bavachinin has anti-tumor effects in vivo, nude mice were inoculated with KB cells to create a tumor, and treated with Bavachinin (5 mg/kg) or vehicle control (PBS), beginning three days after implantation (tumors were 50 mm3). Body weight and tumor growth were measured for 28 day after beginning the treatment. The tumor volume in the control group increased steadily reaching 1800 mm3, a 36-fold increase over four weeks. An intraperitoneal administration of Bavachinin significantly reduced the tumor volume by 40.06% relative to the vehicle only (Fig. 7A and C). During the treatment, Bavachinin showed no full necropsy under histopathological evaluation therefore it's suggested that Bavachinin has no sign of toxicity (Fig. 7B). Although body weights did not differ between control and Bavachinin treated mice, a slight increase in body weight was observed over four weeks, probably due to regular growth. Thus, Bavachinin can block angiogenesis in vivo. To further examine the anti-angiogenic effects of Bavachinin, we analyzed the density of intratumoral microvessels by immunohistochemistry. Tumor sections, 4-μm-thick, were prepared from control and Bavachinin treated mice. The sections were stained with an anti-CD31 antibody to detect microvessels. Bavachinin-treated tumors had fewer vessels of luminal size than control tumors even though there are still small vessels detected in the Bavachinin-treated tumors (Fig. 7D). Furthermore, CD31 staining revealed an aberrant morphology characterized by loosely attached or absent pericytes in Bavachinin-treated mice, suggesting that Bavachinin inhibited tumor angiogenesis in vivo.
Therapeutic effect of Bavachinin on asthma [3]
Th2 cells and IL-4, IL-5 and IL-13 are critical in the pathophysiology of asthma. Based on the significant suppression of Th2 cell differentiation and cytokine production, we studied the potential effect of Bavachinin on asthma in vivo. Bavachinin was administered through oral gavage in PEG400 (50 mg/kg body weight) every day for 7 days starting on the last day of challenge (Figure 2). We observed that the thickness of the bronchial wall and the area of airway smooth muscle were significantly reduced in mice treated with Bavachinin compared with asthmatic mice treated with phosphate-buffered saline (Figure 3a). Treated asthmatic mice demonstrated decreased airway hyperreactivity compared with control mice after challenge (Figure 3a). Furthermore, administration of Bavachinin resulted in a significant downregulation of ACh responsiveness compared with asthmatic mice (Figure 3b). To further confirm the effect of Bavachinin in vivo, serum levels of IL-4 and IgE were also measured. Indeed, treatment by Bavachinin significantly inhibited the serum levels of both IL-4 and IgE, which are hallmarks of asthma (Figure 3c and d). Taken together, our results demonstrate for the first time the therapeutic effect of Bavachinin in an animal model of asthma.
Bavachinin significantly reduces Th2 cytokine expression and cellular infiltration in the lung [3]
To validate the therapeutic effect of Bavachinin, the lung tissues of asthmatic mice were further analyzed. We observed that Bavachinin suppressed Th2 cytokine expression in the lung tissues, with similar patterns for IL-4, IL-5 and IL-13 (Figure 4a). We also assessed the infiltration of eosinophils and neutrophils in the lung. The numbers of eosinophils and neutrophils in the lung interstitium were significantly reduced after administration of the compound compared with the asthmatic mice (Figure 4b). Our results further support the therapeutic effect of Bavachinin on the pathogenesis of asthma through altering the local cytokine expression.
Treatment with Bavachinin selectively reduces systemic Th2 cytokine levels [3]
To test the effect of Bavachinin on the global impact of CD4+ T-cell differentiation, splenocytes from asthmatic mice were activated with PMA/ionomycin for intracellular cytokine staining. Treatment with Bavachinin significantly reduced IL-4, IL-5 and IL-13 production from CD4+ T cells, whereas IFN-λ and IL-17 production was not affected (Figure 5). In summary, administration with Bavachinin selectively altered the Th2 differentiation induced by OVA immunization.
BVC/Bavachinin exhibited glucose-lowering properties without inducing weight gain and hepatotoxicity. Importantly, BVC synergised with thiazolidinediones, which are synthetic PPAR-γ agonists, and fibrates, which are PPAR-α agonists, to induce PPAR transcriptional activity, as well as to lower glucose and triacylglycerol levels in db/db mice. We further found that BVC occupies a novel alternative binding site in addition to the canonical site of synthetic agonists of PPAR, and that the synthetic PPAR-γ agonist rosiglitazone can block BVC binding to this canonical site but not to the alternative site. Conclusions/interpretation: This is the first report of a synergistic glucose- and lipid-lowering effect of BVC/Bavachinin and synthetic agonists induced by unique binding with PPAR-γ or -α. This combination may improve the efficacy and decrease the toxicity of marketed drugs for use as adjunctive therapy to treat the metabolic syndrome [5].
Enzyme Assay
Drug affinity responsive target stability (DARTS) [4]
DARTS was performed as described in our previous study Cells were lysed with M-PER lysis buffer supplemented with 1% phosphatase and protease inhibitors and centrifuged at 16,000 × g for 20 min at 4°C. Next, 10X TNC buffer (50 mM Tris·Cl, 50 mM NaCl, 10 mM CaCl2) was added to the supernatant at room temperature for 10 min. The lysates were incubated with DMSO or BavachininBNN (1, 10 or 100 µM) at room temperature for 1 h, followed by incubation with 0.03 mg/ml pronase at room temperature for 30 min. The proteolysis was stopped using SDS loading buffer. All samples were analyzed by western blotting.
Cellular thermal shift assay (CETSA) [4]
Cells treated with BavachininBNN (10 µM) or DMSO at 37°C for 24 h were collected, and the cell suspension was distributed into 0.2 ml PCR tubes, with 200 µl cell suspension in each tube. The PCR tubes were heated at the designated temperature (42, 45, 48, 51 and 54°C) for 3 min. They were then removed and incubated at 4°C immediately following heating. Cells were then lysed using cell lysis buffer for western and analyzed by western blotting as described in the western blotting methods above.
Measurement of intracellular reactive oxygen species (ROS) [4]
An ROS assay kit was used to measure intracellular ROS accumulation. A549 cells were seeded on 6-well culture plates (8×103 cells/well) and treated with different concentrations of BavachininBNN (10, 20, 40 µM), with or without PPARγ antagonists GW9662 (20 µM) and T0070907 (10 µM). The cells were incubated with 10 µM DCFH-DA for 20 min at 37°C, and images were captured using a fluorescence microscop. Cells were then collected and measured using a SpectraMax iD3 microplate reader at an excitation wavelength of 488 nm and an emission wavelength of 525 nm.
TR-FRET assay [5]
LanthaScreen time-resolved fluorescence resonance energy transfer (TR-FRET) competitive binding or coactivator assays use the ligand-binding domain (LBD) of human nuclear receptors tagged with glutathione S-transferase (GST), the terbium-labelled anti-GST antibody and the fluorescent small molecule or coactivator peptide.
Cell Assay
Immunofluorescence[4]
Cell Types: A549 Cell
Tested Concentrations: 25 μM, 50 μM
Incubation Duration: 24 h
Experimental Results: Shows PPARγ protein levels in the cytoplasm and cytoplasm Bavachinin (25, 50 μM; 24 h) increases PPARγ protein expression[4] . The cell nuclei were Dramatically elevated.
Cell Counting Kit-8 (CCK-8) assay [4]
Both A549 and 16HBE cells were seeded on 96-well culture plates (2×103 cells/well) and the cell culture medium was removed 24 h later. Medium containing different concentrations of BavachininBNN (0, 25, 50, 100 and 150 µmol/l) was added to the cells. Following treatment for 24 h at 37°C, 10 µl CCK-8 solution was added to each well and incubated for 1 h at 37°C with 5% CO2. The absorbance value at 450 nm was then measured using a SpectraMax iD3 microplate reader. The IC50 was calculated by comparing the cell viability with the BNN concentration.
Lactate dehydrogenase (LDH) release assay [4]
A549 cells were seeded on 96-well culture plates (2×103 cells/well) and treated with different concentrations of BavachininBNN (10, 20, 40 or 80 µM) or in the presence of PPARγ antagonists GW9662 (20 µM) and T0070907 (10 µM) for 24 h. Cell culture medium (100 µl) was collected for LDH determination using an LDH cytotoxicity assay kit according to the manufacturer's instructions. Foll owing the reaction, the absorbance was read at a wavelength of 490 nm using the SpectraMax iD3 microplate reader.
Animal Protocol
Animal/Disease Models: Athymic nude mice were inoculated subcutaneously (sc) (sc) with KB cells [2]
Doses: 5 mg/kg
Route of Administration: intraperitoneal (ip) injection
Experimental Results: It demonstrated that the tumor volume was Dramatically diminished by 40.06%, and the lumen size and blood vessels were less. 3].

Animal/Disease Models: Asthma mice [3]
Doses: 50 mg/kg
Route of Administration: po (oral gavage)
Experimental Results: demonstrated significant inhibition of serum IL-4 and IgE levels.
Toxicity/Toxicokinetics
mouse LD oral >1 gm/kg Indian Drugs., 29(662), 1992
References

[1]. Isobavachalcone and bavachinin from Psoraleae Fructus modulate Aβ42 aggregation process through different mechanisms in vitro. FEBS Lett. 2013 Sep 17;587(18):2930-5.

[2]. Anti-angiogenic and anti-tumor activity of Bavachinin by targeting hypoxia-inducible factor-1α. Eur J Pharmacol. 2012 Sep 15;691(1-3):28-37.

[3]. Treatment of allergic inflammation and hyperresponsiveness by a simple compound, Bavachinin, isolated from Chinese herbs. Cell Mol Immunol. 2013 Nov;10(6):497-505.

[4]. Bavachinin exhibits antitumor activity against non small cell lung cancer by targeting PPARγ. Mol Med Rep. 2019 Sep;20(3):2805-2811.

[5]. Bavachinin, as a novel natural pan-PPAR agonist, exhibits unique synergistic effects with synthetic PPAR-γ and PPAR-α agonists on carbohydrate and lipid metabolism in db/db and diet-induced obese mice. Diabetologia. 2016 Jun;59(6):1276-86.

Additional Infomation
Bavachinin is a member of flavanones.
Bavachinin has been reported in Cullen corylifolium with data available.
See also: Cullen corylifolium fruit (part of).
Spontaneous aggregation of Aβ is a key factor in the development of Alzheimer's disease. In searching for Aβ aggregation inhibitors from traditional Chinese herbal medicines, we identified two active compounds from Psoraleae Fructus, namely isobavachalcone and bavachinin. We further demonstrated that the two compounds modulate Aβ42 aggregation process through different mechanisms. Isobavachalcone significantly inhibits both oligomerization and fibrillization of Aβ42, whereas bavachinin inhibits fibrillization and leads to off-pathway aggregation. Both of the compounds attenuated Aβ42-induced toxicity in a SH-SY5Y cell model. These findings may provide valuable information for new drug development and Alzheimer's therapy in the future. [1]
Hypoxia-inducible factor-1 (HIF-1) consists of two subunits, the HIF-1β, which is constitutively expressed, and HIF-1α, which is oxygen-responsive. HIF-1α is over-expressed in response to hypoxia, increasing transcriptional activity linked to tumor progression, angiogenesis, metastasis, and invasion. This study aimed to demonstrate that the natural compound, Bavachinin, has potent anti-angiogenic activity in vitro and in vivo. Bavachinin inhibited increases in HIF-1α activity in human KB carcinoma (HeLa cell derivative) and human HOS osteosarcoma cells under hypoxia in a concentration-dependent manner, probably by enhancing the interaction between von Hippel-Lindau (VHL) and HIF-1α. Furthermore, Bavachinin decreased transcription of genes associated with angiogenesis and energy metabolism that are regulated by HIF-1, such as vascular endothelial growth factors (VEGF), Glut 1 and Hexokinase 2. Bavachinin also inhibited tube formation in human umbilical vein endothelial cells (HUVECs) as well as in vitro migration of KB cells. In vivo studies showed that injecting Bavachinin thrice weekly for four weeks significantly reduced tumor volume and CD31 expression in nude mice with KB xenografts. These data indicate that Bavachinin could be used as a therapeutic agent for inhibiting tumor angiogenesis.[2]
Asthmatic inflammation is mediated by a type 2 helper T cell (Th2) cytokine response, and blocking Th2 cytokine production is proven to have a potent therapeutic effect against asthmatic inflammation. Using IL-4-green fluorescent protein (GFP) reporter mice, we demonstrated that Bavachinin, a single compound isolated from a Chinese herb, significantly inhibited Th2 cytokine production, including IL-4, IL-5 and IL-13. Notably, this compound almost completely blocked inflammation in the ovalbumin (OVA)-sensitized animal asthma model. Furthermore, we demonstrated that this chemical selectively affects the level of GATA-3, most likely by affecting the stability of GATA-3 mRNA. Our results demonstrate, for the first time, the potential therapeutic value of this single compound derived from Chinese herbs.[3]
Aims/hypothesis: Pan-peroxisome proliferator-activated receptor (PPAR) agonists have long been sought as therapeutics against the metabolic syndrome, but current PPAR agonists show limited efficacy and adverse effects. Natural herbs provide a structurally untapped resource to prevent and treat complicated metabolic syndrome. Methods: Natural PPAR agonists were screened using reporter gene, competitive binding and 3T3-L1 pre-adipocyte differentiation assays in vitro. The effects on metabolic phenotypes were verified in db/db and diet-induced obese mice. In addition, potentially synergistic actions of bavachinin (BVC, a novel natural pan-PPAR agonist from the fruit of the traditional Chinese glucose-lowering herb malaytea scurfpea) and synthetic PPAR agonists were studied through nuclear magnetic resonance, molecular docking, reporter gene assays and mouse studies.[5]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C21H22O4
Molecular Weight
338.3970
Exact Mass
338.151
CAS #
19879-30-2
PubChem CID
10337211
Appearance
White to light yellow solid powder
Density
1.2±0.1 g/cm3
Boiling Point
537.1±50.0 °C at 760 mmHg
Melting Point
139-145ºC
Flash Point
190.3±23.6 °C
Vapour Pressure
0.0±1.5 mmHg at 25°C
Index of Refraction
1.590
LogP
4.93
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
4
Heavy Atom Count
25
Complexity
488
Defined Atom Stereocenter Count
1
SMILES
CC(=CCC1=CC2=C(C=C1OC)O[C@@H](CC2=O)C3=CC=C(C=C3)O)C
InChi Key
VOCGSQHKPZSIKB-FQEVSTJZSA-N
InChi Code
InChI=1S/C21H22O4/c1-13(2)4-5-15-10-17-18(23)11-20(14-6-8-16(22)9-7-14)25-21(17)12-19(15)24-3/h4,6-10,12,20,22H,5,11H2,1-3H3/t20-/m0/s1
Chemical Name
(2S)-2,3-dihydro-2-(4-hydroxyphenyl)-7-methoxy-6-(3-methyl-2-buten-1-yl)-4H-1-benzopyran-4-one
Synonyms
7-O-Methylbavachin; Bavachinin; 19879-30-2; Bavachinin A; 7-O-Methylbavachin; 4H-1-Benzopyran-4-one, 2,3-dihydro-2-(4-hydroxyphenyl)-7-methoxy-6-(3-methyl-2-buten-1-yl)-, (2S)-; VL3EV483SZ; UNII-VL3EV483SZ; BRN 3629340;
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO : ~125 mg/mL (~369.39 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (6.15 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.08 mg/mL (6.15 mM) (saturation unknown) in 10% DMSO + 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 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.9551 mL 14.7754 mL 29.5508 mL
5 mM 0.5910 mL 2.9551 mL 5.9102 mL
10 mM 0.2955 mL 1.4775 mL 2.9551 mL

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