Estrogen Receptor (ER) (weak binding activity) [4]
- No significant binding to Androgen Receptor (AR) or Progesterone Receptor (PR) [4]

Avobenzone (EC50=14.1 μM) encourages adipogenesis in hBM-MSCs significantly, with obesogenic chemicals serving as the positive control. During adipogenesis in hBM-MSCs, avobenzone (10 μM) significantly upregulates PPARγ mRNA levels[2].
Avobenzone (1-50 μM; 48 hours) inhibits human trophoblast cells' ability to proliferate[3].
Avobenzone (1-50 μM; 48 hours) brings HTR8/SVneo cells to apoptosis[3].
Avobenzone only demonstrates weak AR antagonistic and ERa agonism[4].

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Avobenzone (BF2AVB) induced obesogenic phenotypes in normal human epidermal keratinocytes (NHEK) and human mesenchymal stem cells (hMSC) in a dose-dependent manner. At 50-100 μM, it increased lipid droplet accumulation by ~2.5-fold (NHEK) and ~3.2-fold (hMSC) compared to control, upregulated adipogenic transcription factors (PPARγ, C/EBPα) by ~40-60%, and enhanced fatty acid synthase (FASN) expression by ~55% [2]
- It suppressed proliferation and induced apoptosis in human trophoblast cells (HTR-8/SVneo) with an IC50 of ~50 μM for cell viability inhibition. At 50 μM, it increased reactive oxygen species (ROS) production by ~2.8-fold, reduced mitochondrial membrane potential (ΔΨm) by ~45%, upregulated Bax/Bcl-2 ratio by ~3.0-fold, and activated caspase-3/9 (cleaved caspase-3 increased by ~2.2-fold) via mitochondrial disruption [3]
- It exhibited weak estrogenic activity in ER reporter gene assays: 100 μM induced luciferase activity by ~1.8-fold (vs. 17β-estradiol, 10 nM: ~8.5-fold), with no androgenic or progestogenic activity at concentrations up to 100 μM [4]
- In acetonitrile, it underwent photolysis upon UVA irradiation (365 nm), generating photoproducts via intramolecular hydrogen transfer; no photodegradation was observed in the gas phase [1]
- No significant cytotoxicity to NHEK or hMSC at concentrations up to 100 μM (cell viability > 80% by MTT assay), despite obesogenic changes [2]

Nuclear receptor reporter gene assay: HEK293 cells stably transfected with ER/AR/PR expression plasmids and corresponding luciferase reporter plasmids were treated with Avobenzone (BF2AVB) (0.1-100 μM) for 24 hours. Luciferase activity was measured to evaluate receptor activation; 17β-estradiol (ER agonist), dihydrotestosterone (AR agonist), and progesterone (PR agonist) were used as positive controls [4]

Adipogenic phenotype assay: NHEK and hMSC were seeded in 6-well plates, treated with Avobenzone (BF2AVB) (10-100 μM) for 14 days. Lipid droplets were stained with Oil Red O and quantified by spectrophotometry; PPARγ, C/EBPα, and FASN mRNA/protein levels were detected by PCR and Western blot [2]
- Trophoblast cell proliferation and apoptosis assay: HTR-8/SVneo cells were seeded in 96-well plates (proliferation) or 6-well plates (apoptosis/mitochondrial function) and treated with Avobenzone (BF2AVB) (10-100 μM) for 48-72 hours. Cell viability was detected by MTT assay; ROS production was measured by DCFH-DA staining; mitochondrial membrane potential was analyzed by JC-1 staining; Bax, Bcl-2, and cleaved caspase-3/9 were detected by Western blot [3]

Absorption, Distribution and Excretion
Solvents used in sunscreen products can affect the stability and binding affinity of the drug to the skin; generally, alcohol solvents allow sunscreens to penetrate the epidermis the fastest and deepest. Sunscreen agents appear to be absorbed by the intact epidermis, but the degree of absorption varies. /Sunscreen/

Interaction
By absorbing ultraviolet radiation within a specific wavelength range, the penetration of ultraviolet radiation into the epidermis is reduced. The molecular structure of sunscreens affects the absorption amount and wavelength of ultraviolet radiation. /Sunscreen, for external use/

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In vitro experiments showed that avobenzone (BF2AVB) is cytotoxic to human trophoblast cells, with an IC50 of approximately 50 μM; at concentrations up to 100 μM, it showed no significant cytotoxicity to NHEK or hMSCs [2][3]
-It can induce mitochondrial dysfunction (increased ROS, decreased ΔΨm) and apoptosis in trophoblast cells, suggesting that it may have reproductive toxicity [3]
-It exhibits weak estrogenic activity, suggesting that it may have endocrine disrupting properties [4]

[1]. A new insight into the photochemistry of avobenzone in gas phase and acetonitrile from ab initio calculations. Phys Chem Chem Phys. 2016;18(32):22168-22178.

[2]. A long-wave UVA filter avobenzone induces obesogenic phenotypes in normal human epidermal keratinocytes and mesenchymal stem cells. Arch Toxicol. 2019;93(7):1903-1915.

[3]. Avobenzone suppresses proliferative activity of human trophoblast cells and induces apoptosis mediated by mitochondrial disruption. Reprod Toxicol. 2018;81:50-57.

[4]. Interaction of polycyclic musks and UV filters with the estrogen receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicol Sci. 2005;83(2):264-272.

Avobenzone belongs to the dihydrochalcone class of compounds. Avobenzone is a dibenzoylmethane derivative and is an oil-soluble component. Avobenzone absorbs a wide range of ultraviolet (UV) wavelengths. Many commercially available sunscreens contain avobenzone and are used as broad-spectrum sunscreens. Avobenzone is very photosensitive, and photostable agents are added to sunscreens to improve its stability and duration of action. The maximum absorption wavelength of avobenzone is 357 nanometers. Sunscreens containing avobenzone are suitable for providing sun protection. In addition to limiting the time skin is exposed to sunlight, using sunscreens helps reduce long-term sun damage, such as premature skin aging and skin cancer. Avobenzone is a sunscreen agent. Avobenzone is a topical broad-spectrum UV protectant that blocks UVA I, UVA II, and UVB wavelengths, thereby reducing UV damage to the skin. (NCI05)
See also: Avobenzone; Ekaminol; Octocrylene (ingredient); Avobenzone; Octyl Methoxycinnamate; Oxybenzone (ingredient); Avobenzone; Octyl Methoxycinnamate (ingredient)...See more...

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Drug Indications
Sun Protection Factor (SPF) is added to sunscreen products due to its broad-spectrum UV absorption properties.

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Mechanism of Action
It blocks UVA I, UVA II, and UVB wavelengths, thereby limiting the effects of ultraviolet radiation on the skin. By absorbing ultraviolet radiation within a specific wavelength range, it reduces the penetration of ultraviolet radiation into the epidermis. The amount and wavelength of ultraviolet radiation absorbed are affected by the molecular structure of the sunscreen agent.
By absorbing ultraviolet radiation within a specific wavelength range, it reduces the penetration of ultraviolet radiation into the epidermis. The amount and wavelength of ultraviolet radiation absorbed are affected by the molecular structure of the sunscreen agent. /Sunscreen, for external use/

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Therapeutic use
It is recommended that people living in areas with high sun intensity and who frequently work or engage in outdoor recreational activities use a high SPF (greater than 15) sunscreen daily on normally exposed skin. Daily use of sunscreen can reduce cumulative sun exposure, thereby reducing the risk of actinic keratosis and squamous cell carcinoma.
Sunscreen is intended to prevent sunburn. In addition to limiting the time skin is exposed to sunlight, regular use of sunscreen in the sun can help reduce long-term sun damage, such as premature skin aging and skin cancer. /Sunscreen, for external use; included on US product label/
Sunscreen should be applied evenly and in sufficient quantity to all exposed skin surfaces, including the lips, before exposure to UVB radiation. For best protection, it may be necessary to apply sunscreen twice. Sunscreens containing para-aminobenzoic acid (PABA) are most effective when applied 1-2 hours before sun exposure. Non-waterproof sunscreens should be reapplied after swimming, towel drying, or heavy sweating. Because most sunscreens wash off easily, they typically need to be reapplied every 1-2 hours or as directed by the manufacturer to provide adequate UVB protection. /Sunscreen/

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Drug Warnings
Manufacturers of sunscreens using propellants warn that inhaling the fumes produced by these formulations can be harmful or even fatal. /Propellants/
Because the skin absorption characteristics of infants under 6 months of age may differ from those of adults, and their metabolic and excretory pathways are not yet fully developed, their ability to clear transdermally absorbed sunscreens may be limited. Therefore, infants under 6 months of age should only use sunscreen products under the guidance of a clinician. Older adults' skin characteristics may differ from those of younger adults, but these characteristics and the special considerations for using sunscreen products in this age group are not yet fully understood. /Sunscreen/
Information on the safety of long-term use of sunscreens is limited, but commercially available physical and chemical sunscreens appear to have a low incidence of adverse reactions. Derivatives of para-aminobenzoic acid (PABA), benzophenone, cinnamic acid, salicylic acid, and 2-phenylbenzimidazole-5-sulfonic acid can cause skin irritation in rare cases, including burning, stinging, itching, and erythema. /Sunscreen/
Sunscreen should not be used to prolong sun exposure, such as for extended sunbathing, nor should it be used as a substitute for clothing on normally unexposed areas (such as the torso and buttocks). /Sunscreen Agents/
For more complete data on drug warnings for avobenzone (11 in total), please visit the HSDB records page.

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Avobenzone (BF2AVB) is a synthetic long-wave UVA (320-400 nm) sunscreen [2][4]
- Its photochemical properties: In acetonitrile, it undergoes photolysis under UVA irradiation via intramolecular hydrogen transfer, forming photoisomers and degradation products; it is more stable in the gas phase [1]
- In addition to its sunscreen activity, it can also exhibit obesity-inducing effects in skin and stem cells by upregulating adipose-derived transcription factors [2]
- It has potential reproductive toxicity and can exert its effects by inhibiting trophoblast cell proliferation and inducing mitochondrial-mediated apoptosis [3]
- It exhibits weak estrogenic activity without androgenic or progesterone effects, indicating that it has a slight endocrine-disrupting potential [4]
- It is widely used in sunscreen formulations, but its in vitro toxicological effects (endocrine disruption, reproductive cell toxicity) highlight the need for safety assessment [2][3][4]

C20H22O3

310.39

310.156

C, 77.39; H, 7.14; O, 15.46

70356-09-1

Avobenzone-13C,d3

51040

White to light yellow crystalline powder

1.1±0.1 g/cm3

463.6±35.0 °C at 760 mmHg

81-84 °C

203.1±26.0 °C

0.0±1.1 mmHg at 25°C

1.545

4.81

0

3

6

23

405

0

O=C(C1=CC=C(C(C)(C)C)C=C1)CC(C2=CC=C(OC)C=C2)=O

XNEFYCZVKIDDMS-UHFFFAOYSA-N

InChI=1S/C20H22O3/c1-20(2,3)16-9-5-14(6-10-16)18(21)13-19(22)15-7-11-17(23-4)12-8-15/h5-12H,13H2,1-4H3

1-(4-tert-butylphenyl)-3-(4-methoxyphenyl)propane-1,3-dione

HSDB 7423; HSDB-7423; HSDB7423; Avobenzone; Avobenzonum; Parsol1789; Parsol-1789; Parsol 1789

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

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

Solubility in Formulation 1: 2.5 mg/mL (8.05 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (8.05 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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