TBPH
Based on 1 Customer Validation
TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis.
For research use only. We do not sell to patients.
- Purity : 95.0%
- CAS No.: 26040-51-7
- Formula: C24H34Br4O4
- Molecular Weight:706.14
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Storage:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
TBPH (5-50 μM, 48 h) promotes NASH progression by disrupting MFN2-regulated ER-Mito contacts in NASH LOs model[1].
TBPH (0-20 μg/mL, 48 h) decreases cell proliferation ability, causes oxidative stress, increase lung tissue fibrosis, causes the release of ds-DNA from lung mitochondria, which activates c-GAS-STING in TC-1 and BEAS-2B cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:NASH LOs model
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Concentration:5 μM, 50 μM
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Incubation Time:48 h
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Result:Upregulated the transcriptional levels of oxidative stress-related genes (CYP2E1 and CYP1A2), fibrosis-related genes (COL3A1, COL4A1, LOXL2, TIMP1, VIM), and inflammation-related genes (TNF-α, IL-8).
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Cell Line:NASH LOs model
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Concentration:5 μM, 50 μM
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Incubation Time:48 h
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Result:Decreased colocalization of mitochondria (HSP60) and ER (GRP78), indicating reduced ER-Mito contacts.
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Cell Line:NASH LOs model
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Concentration:5 μM, 50 μM
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Incubation Time:48 h
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Result:Decreased MFN2 level, increased UPRmt markers (HSP60, SOD2) and ER stress markers (GRP78, ATF6).
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Cell Line:TC-1 and BEAS-2B cells
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Concentration:0 μg/mL, 0.2 μg/mL, 2 μg/mL, 10 μg/mL
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Incubation Time:48 h
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Result:Inhibited the expression of CyclinD1 and promoted the phosphorylation of Rb, increased the expression levels of CDK2/4 and P53.
Increased the levels of IL-6, IL-1β, p-IκB and p-P65.
Up-regulated the expression of FN and α-SMA, Down-regulated the expression of E-cadherin.
In Vivo
TBPH (20-200 mg/kg, i.g., once a day, 4 weeks) does not alter liver morphology and does not change the hepatosomatic index, but impairs hepatocytic ER-Mito contacts, induces mitochondrial dysfunction and ER stress in normal diet (ND) mice model[1].
TBPH (0-100 μg/mL, i.g., once a day, 4 weeks) causes oxidative damage to lung cells and triggers inflammatory responses in lung cells and tissues in C57 mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:MCD diet-induced NASH mouse (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
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Dosage:20 mg/kg, 200 mg/kg
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Administration:i.g., once a day, 4 weeks
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Result:Exacerbated hepatic pathology, increased the hepatosomatic index, enhanced lipid accumulation, decreased serum HDL and CHO levels, alongside elevated hepatic TG and serum LDL levels.
Augmented hepatic steatosis and inflammatory cell infiltration, enhanced fibrotic deposition, increased steatosis, inflammatory infiltration, fibrosis and NASH scores, elevated serum levels of AST and ALT.
Reduced the abundance of cardiolipin (CL), phosphatidylserine (PS), and phosphatidylethanolamine (PE), while increasing phosphatidic acid (PA) levels.
Disrupted lipid metabolism associated with the endoplasmic reticulum and mitochondria, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Caused a marked reduction in mitochondrial cristae, disrupted cristae junctions (CJs), and disorganization of cristae membranes in hepatocytes, reduced overall oxygen consumption and ATP content.
Increased HSP60, SOD2, mitochondrial proteases (LONP1, ClpP), GRP78, Atf6, eIF2α, and Chop levels, decreased the MFN2 protein level.
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Animal Model:ND mice (Male C57BL/6, 8-9 weeks old, 22-25 g) model[1]
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Dosage:20 mg/kg, 200 mg/kg
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Administration:i.g., once a day, 4 weeks
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Result:Did not significantly alter liver morphology, did not change the hepatosomatic index.
Affected C14:0 metabolism, fatty acids with 13-15 carbon chains, and mitochondrial metabolic processes, altered the negative intrinsic curvature of membranes.
Reduced colocalization of ER and mitochondria in liver tissues, increased the physical distance between ER and mitochondria and reduced contact sites.
Elevated the protein levels of mitochondrial chaperone HSP60, SOD2, GRP78, Atf6, eIF2α, and Chop, decreased the MFN2 protein level.
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Animal Model:C57 mice model[2]
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Dosage:0 μg/mL, 0.5 μg/mL, 1 μg/mL, 5 μg/mL, 10 μg/mL, 30 μg/mL L, 60 μg/mL, 100 μg/mL
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Administration:i.g., once a day, 4 weeks
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Result:Induced capillary congestion in the alveolar wall and obvious inflammatory cell infiltration.
Increased the expression levels of TNFα, IL-1β, IL-6, IL-8, IFNγ, eotaxin, MCP-1, MIP-2, RANTES, p16, p21, P65, and p-IκB proteins, and decreased the expression level of cell proliferation marker (Ki67).
Up-regulated the expression of FN, α-SMA, and TGF-β, down-regulated the expression of E-cadherin, and increases the content of collagen fibers in the lungs.
Increased ROS and MDA levels, and decreased GSH, SOD, and CAT expression levels.
Chemical Information
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CAS No. 26040-51-7
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Appearance Liquid (Density: 1.529±0.06 g/cm3)
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Molecular Weight 706.14
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Formula C24H34Br4O4
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Color Light yellow to yellow
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SMILES
O=C(OCC(CC)CCCC)C1=C(Br)C(Br)=C(Br)C(Br)=C1C(OCC(CC)CCCC)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
Solvent & Solubility
In Vitro:
DMSO : ≥ 175 mg/mL (247.83 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
* "≥" means soluble, but saturation unknown.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
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).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
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.
Protocols
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Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
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Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
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Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
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Mitochondrial membrane-potential and mitochondrial mass staining
Mitochondrial membrane potential staining measures the electrochemical polarization across the mitochondrial inner membrane in live cells using lipophilic cationic fluorescent probes; early rhodamine-based work showed that selective mitochondrial dye accumulation is lost when the mitochondrial transmembrane potential is dissipated. JC-1 reports mitochondrial polarization by shifting from green monomer fluorescence to red J-aggregate fluorescence as dye concentration increases within energized mitochondria; therefore, the red/green fluorescence ratio is used as a relative readout of mitochondrial membrane potential. TMRE or TMRM staining provides a single-channel relative readout because these cationic rhodamine esters accumulate in polarized mitochondria, and lower fluorescence indicates reduced mitochondrial polarization when acquisition and dye-loading conditions are controlled. Mitochondrial mass staining is commonly performed with MitoTracker Green FM or related MitoTracker dyes as
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Inhalation Toxicity Study
Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Purity & Documentation
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Data Sheet (286 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Zhou Y, Li B, Zhao J, Ren X, Guo Y, Yang L, Han J, Wu L, Zhou B. Bis(2-Ethylhexyl)-2,3,4,5-Tetrabromophthalate Promotes NASH Progression through Disrupting Endoplasmic Reticulum-Mitochondria Contacts. Environ Sci Technol. 2025 Jul 22;59(28):14302-14313. [Content Brief]
[2]. Xing B, et al. TBPH-induced lung injury is induced by mitochondrial-derived ds-DNA-mediated inflammatory response. Ecotoxicol Environ Saf. 2024 Nov 1;286:117200. [Content Brief]
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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 1.4161 mL | 7.0807 mL | 14.1615 mL | 35.4037 mL |
| 5 mM | 0.2832 mL | 1.4161 mL | 2.8323 mL | 7.0807 mL | |
| 10 mM | 0.1416 mL | 0.7081 mL | 1.4161 mL | 3.5404 mL | |
| 15 mM | 0.0944 mL | 0.4720 mL | 0.9441 mL | 2.3602 mL | |
| 20 mM | 0.0708 mL | 0.3540 mL | 0.7081 mL | 1.7702 mL | |
| 25 mM | 0.0566 mL | 0.2832 mL | 0.5665 mL | 1.4161 mL | |
| 30 mM | 0.0472 mL | 0.2360 mL | 0.4720 mL | 1.1801 mL | |
| 40 mM | 0.0354 mL | 0.1770 mL | 0.3540 mL | 0.8851 mL | |
| 50 mM | 0.0283 mL | 0.1416 mL | 0.2832 mL | 0.7081 mL | |
| 60 mM | 0.0236 mL | 0.1180 mL | 0.2360 mL | 0.5901 mL | |
| 80 mM | 0.0177 mL | 0.0885 mL | 0.1770 mL | 0.4425 mL | |
| 100 mM | 0.0142 mL | 0.0708 mL | 0.1416 mL | 0.3540 mL |
TBPH Related Classifications
HY-W018587 Related Classifications
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