| Size | Price | Stock | Qty |
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| 50mg |
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| Other Sizes |
| Targets |
The primary target of BF-175 is SIRT1 (NAD-dependent deacetylase sirtuin-1), a class III histone deacetylase (HDAC) that requires NAD+ for its catalytic activity. SIRT1 deacetylates various protein substrates involved in cellular regulation, energy metabolism, stress resistance, and aging. By acting as a SIRT1 agonist, BF-175 enhances SIRT1‘s deacetylase activity, leading to activation of PGC1-alpha (a master regulator of mitochondrial biogenesis), inhibition of SREBP (a key transcription factor for lipid metabolism), induction of autophagy, and modulation of apoptosis pathways. BF-175 also acts as an AR (androgen receptor) antagonist and an SREBF1 (sterol regulatory element-binding transcription factor 1) inhibitor based on some databases. These multi-target activities contribute to its diverse pharmacological effects.
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| ln Vitro |
In cell-free assays, BF-175 functions as a selective SIRT1 agonist, enhancing the deacetylase activity of SIRT1. Specific IC50 or EC50 values are not reported in the available literature, but the compound‘s activity is characterized by increased SIRT1-mediated deacetylation of target proteins such as PGC1-alpha. As a SIRT1 agonist, BF-175 may act through an allosteric mechanism, enhancing the enzyme‘s catalytic efficiency rather than competing with the substrate or NAD+ cofactor. The compound‘s selectivity for SIRT1 over other sirtuin isoforms (SIRT2-7) and other HDAC families has not been fully characterized in available sources, but it is described as selective.
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| ln Vivo |
In vitro, BF-175 has demonstrated several biological activities. It enhances SIRT1-mediated activation of PGC1-alpha, leading to increased mitochondrial biogenesis and function. BF-175 induces apoptosis in cancer cells (e.g., endometrial carcinoma cells) and induces autophagy, likely through SIRT1-mediated deacetylation of autophagy-related proteins (such as LC3, ATG proteins, or FOXO transcription factors). The compound inhibits SREBP activity, resulting in reduced lipogenesis and lipid accumulation. BF-175 protects against high glucose-mediated mitochondrial injury in cell culture models, suggesting potential benefits in diabetic conditions. In endometrial carcinoma cell lines, BF-175 inhibits cell proliferation and induces cell death, demonstrating anti-cancer activity. Detailed cellular endpoints: SIRT1 activity (acetylation status of SIRT1 substrates), PGC1-alpha activity, mitochondrial membrane potential (JC-1 staining), reactive oxygen species (ROS) levels, apoptosis (Annexin V/PI, caspase-3/7 activation), autophagy (LC3-II accumulation, p62 levels), and SREBP target gene expression (FASN, SCD1).
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| Enzyme Assay |
In vivo, BF-175 demonstrates protective effects against high glucose-mediated mitochondrial injury and delays the progression of diabetic kidney disease (DKD) in animal models. While detailed in vivo animal experimental protocols for BF-175 are limited in the available literature, the compound has been studied in models of diabetes and diabetic complications. Typical endpoints in DKD models include: blood glucose levels, urinary albumin excretion (UAE), serum creatinine and blood urea nitrogen (BUN) levels, renal histopathology (glomerular basement membrane thickness, mesangial expansion, tubulointerstitial fibrosis), and markers of mitochondrial injury and oxidative stress. BF-175 also inhibits endometrial carcinoma in vivo, suggesting anti-tumor activity in xenograft models. The compound may be administered orally or intraperitoneally at doses likely ranging from 5-50 mg/kg.
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| Cell Assay |
Not specifically reported for BF-175 in the available literature. For SIRT1 agonist characterization, typical non-cell-based assays measure SIRT1 deacetylase activity. Purified recombinant human SIRT1 is incubated with a fluorogenic acetylated peptide substrate (e.g., Ac-Gln-Arg-Ser-Thr-Lys(Ac)-Lys-Lys-AMC, derived from p53) and NAD+. The deacetylation reaction generates AMC fluorescence (excitation ~360 nm, emission ~460 nm). BF-175 is added at varying concentrations (0.1 nM - 100 microM) to determine EC50 for SIRT1 activation. Selectivity is assessed using analogous assays with other sirtuins (SIRT2-7) using specific peptide substrates. Alternatively, an ADP-Glo SIRT1 assay measures NAD+ consumption. The SIRT1 agonist activity is confirmed by measuring increased deacetylation of a recombinant SIRT1 substrate protein in the presence of BF-175.
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| Animal Protocol |
For BF-175, cell-based assays typically involve various cell lines depending on the biological endpoint. For diabetic kidney disease research, primary podocytes or renal tubular epithelial cells (e.g., HK-2 cells) are used. Cells are cultured in high-glucose medium (e.g., 25-30 mM glucose) to model diabetic conditions, then treated with BF-175 (0.1-20 microM) for 24-72 hours. Endpoints: mitochondrial function (MTT, JC-1 staining, ATP levels, ROS production), apoptosis (Annexin V/PI, TUNEL, caspase-3/7 activation), autophagy (LC3-II/I ratio, p62 levels by Western blotting, autophagosome formation by transmission electron microscopy), SIRT1 activity (acetylation status of PGC1-alpha, p53, FOXO by immunoprecipitation and Western blotting), and expression of SREBP target genes (qRT-PCR). For endometrial carcinoma research, endometrial cancer cell lines (e.g., Ishikawa, HEC-1A, KLE) are cultured in standard medium and treated with BF-175 for 24-72 hours; cell viability is measured by MTT/CCK-8, and apoptosis is assessed by flow cytometry.
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| ADME/Pharmacokinetics |
In vivo protocols for BF-175 would depend on the disease model. For diabetic kidney disease (DKD) research, male C57BL/6 mice or rats are rendered diabetic by injection of streptozotocin (STZ, 50-60 mg/kg intraperitoneally for 5 consecutive days) or by using genetically diabetic models (e.g., db/db mice, Otsuka Long-Evans Tokushima Fatty rats). Once diabetes is confirmed (blood glucose >250 mg/dL), BF-175 is administered orally (by gavage) at doses of 5-30 mg/kg daily for 4-12 weeks. Endpoints: blood glucose and HbA1c measurements, urine albumin-to-creatinine ratio (UACR), serum creatinine and BUN, kidney weight-to-body weight ratio, renal histology (PAS staining for mesangial expansion, Masson‘s trichrome for fibrosis, electron microscopy for glomerular basement membrane thickness), immunohistochemistry for oxidative stress markers (4-HNE, 8-OHdG) and fibrotic markers (fibronectin, collagen IV), and Western blotting for SIRT1/PGC1-alpha signaling. For endometrial carcinoma models, female nude mice are injected subcutaneously with endometrial cancer cells; BF-175 is administered when tumors reach ~100 mm3, and tumor growth is monitored for 2-4 weeks.
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| Toxicity/Toxicokinetics |
Not specifically reported for BF-175 in the available literature. The compound is described as orally active, indicating sufficient absorption following oral administration. As a small molecule SIRT1 agonist, it likely has moderate to high oral bioavailability, moderate plasma protein binding, moderate clearance (likely hepatic metabolism), and moderate half-life (2-8 hours in rodents). Detailed PK parameters such as F (%), half-life, volume of distribution, Cmax, Tmax, clearance, and AUC have not been reported in the available literature. BF-175 is used in preclinical models of diabetic kidney disease and endometrial carcinoma, suggesting it achieves sufficient systemic exposure and target engagement at efficacious doses.
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| References | |
| Additional Infomation |
Specific toxicity data for BF-175 are not extensively reported in the available literature. The compound is intended for research use only and not for human therapeutic applications. As a SIRT1 agonist, potential on-target toxicities could include effects on metabolism, cell survival, and inflammation. SIRT1 activation has been associated with both beneficial and adverse effects depending on context. Off-target effects on other sirtuins or HDACs cannot be excluded. BF-175 also has activity as an AR antagonist and SREBF1 inhibitor, which could contribute to endocrine and metabolic toxicities. In preclinical efficacy studies, BF-175 was reportedly well-tolerated at efficacious dose levels, with no severe acute toxicity reported. Standard safety precautions for handling should be observed, including use of appropriate personal protective equipment, working in a fume hood, and avoiding inhalation or skin contact.
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| Molecular Formula |
C20H21BCL2O2
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| Molecular Weight |
375.10
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| CAS # |
1333375-02-2
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| Appearance |
Typically exists as solids at room temperature
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| HS Tariff Code |
2934.99.9001
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| 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)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.6660 mL | 13.3298 mL | 26.6596 mL | |
| 5 mM | 0.5332 mL | 2.6660 mL | 5.3319 mL | |
| 10 mM | 0.2666 mL | 1.3330 mL | 2.6660 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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