| Size | Price | Stock | Qty |
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| 10mg |
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| 50mg |
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| 100mg |
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| Other Sizes |
| Targets |
5-HT1A Receptor 1 nM (Ki) 5-HT2A Receptor 49 nM (Ki)
Flibanserin targets multiple G protein-coupled receptors (GPCRs) in the central nervous system. Its highest affinity is for the 5-HT1A receptor (Ki = 1 nM), where it acts as a full agonist. It also antagonizes 5-HT2A receptors (Ki = 49 nM) and binds to dopamine D4 receptors (Ki = 4-24 nM). Additionally, it has moderate affinity for 5-HT2B, 5-HT2C, and 5-HT5A receptors but negligible affinity for other serotonin, dopamine, adrenergic, or histamine receptors. The combined effect of 5-HT1A agonism and 5-HT2A antagonism reduces serotonin-mediated inhibition of dopamine and norepinephrine release in brain regions involved in sexual motivation and reward, including the medial preoptic area and ventral tegmental area. |
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| ln Vitro |
Flibanserin (hydrochloride) (propan-2-ol) (hydrate) (0.01-100 μM; 72 h) can transform into two degradation products DP1 and DP2 with no toxicity potential after oxidative degradation[1].
In vitro studies characterize flibanserin's receptor binding and stability profile. Receptor binding affinity is determined using radioligand displacement assays in transfected cell membranes expressing human receptors. The 5-HT1A agonist activity is confirmed via [3⁵S]GTPgammaS binding assays, measuring G protein activation (EC50 ~30 nM). Flibanserin shows no direct cytotoxicity in human primary cells (e.g., NHSF fibroblasts) at concentrations up to 100 microM (72 hours), with IC50 >100 microM for both parent drug and its oxidative degradation products (DP1, DP2). Cell viability remained >96% at all tested concentrations. The compound undergoes oxidative degradation at stressed conditions, forming two major degradants with no increased toxicity potential compared to the parent compound. |
| ln Vivo |
Flibanserin hydrochloride (1, 10, 30 mg/kg; i.p.; single dose) shows different pharmacological properties in prefrontal cortex, hippocampus and midbrain. The 5-HT1A receptor occupancy in cortex indicates it’s the more sensitive than other brain region[2]. Flibanserin hydrochloride (15, 45 mg/kg; p.o.; twice a day; 22 d) preferentially activates the brain regions belonging to the mesolimbic dopaminergic pathway and hypothalamic structures involved in the integration of sexual cues related to sexual motivation[3]. Flibanserin hydrochloride (5, 10, 25, and 50 mg/kg; s.c.; single dose) has anxiolytic effects without locomotor side effects in rat ultrasonic vocalization model[4].
In vivo activity has been extensively characterized in animal models. In female rats, flibanserin (15-45 mg/kg, oral, twice daily for 22 days) preferentially activates brain regions belonging to the mesolimbic dopaminergic pathway and hypothalamic structures involved in sexual cue integration, including the medial preoptic area, arcuate nucleus, and ventral tegmental area. In the rat ultrasonic vocalization model of anxiety, flibanserin (5-50 mg/kg, subcutaneous) demonstrates anxiolytic effects without locomotor side effects. In microdialysis studies, flibanserin (1-30 mg/kg IP) lowers 5-HT while raising dopamine and norepinephrine in the rat prefrontal cortex. The 5-HT1A receptor occupancy in cortex is higher than in hippocampus and midbrain. In humans, flibanserin 100 mg daily at bedtime is approved for HSDD. |
| Enzyme Assay |
Cell-free receptor binding assays: Radioligand competition binding is performed using membranes from CHO or HEK293 cells stably expressing human 5-HT1A, 5-HT2A, or D4 receptors. Membranes (10-50 microg protein) are incubated with [3H]-8-OH-DPAT (for 5-HT1A, 0.5 nM), [3H]-ketanserin (for 5-HT2A, 1 nM), or [3H]-spiperone (for D4, 1 nM) and flibanserin (0.001-10,000 nM) in assay buffer (50 mM Tris-HCl pH 7.4, 120 mM NaCl, 5 mM KCl, 5 mM MgCl2, 1 mM EDTA) for 60-120 minutes at 25-37degC. Non-specific binding is defined with 10 microM serotonin or haloperidol. Bound radioactivity is separated by filtration through GF/B filters and counted by scintillation. Ki values are calculated by Cheng-Prusoff equation. For functional activity (5-HT1A agonism), [3⁵S]GTPgammaS binding assays measure G protein activation.
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: NHSF cell lin Concentration: 0.01, 0.1, 1, 10, 100 μM Incubation Duration: 72 hours Experimental Results: Resulted cell viability reached to 97.91% (DP1) and 96.73% (DP2) at 0.01 μM. Showed non-toxic up to 100 μM (IC50 >100 μM). For cell viability and degradation studies, human neonatal foreskin fibroblasts (NHSF) are cultured in DMEM with 10% FBS, 2 mM L-glutamine, and antibiotics at 37degC in 5% CO2. Cells are seeded in 96-well plates at 5,000-10,000 cells/well. Flibanserin hydrochloride (propan-2-ol) hydrate is dissolved in DMSO (final concentration ≤0.5%) and added at concentrations of 0.01, 0.1, 1, 10, and 100 microM for 72 hours. Cell viability is assessed by MTT assay (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide). Absorbance is measured at 570 nm (reference 630 nm). Cell viability remains >96% at all concentrations (IC50 >100 microM). Oxidative degradation studies: The compound is subjected to stress conditions (0.1% H2O2, 24 hours), and degradation products DP1 and DP2 are analyzed by HPLC and tested similarly. |
| Animal Protocol |
Animal/Disease Models:Long Evans female rats (225-250 g)[3]
Doses: 15 mg/kg; 45 mg/kg Route of Administration: Oral gavage; twice a day for 22 days Experimental Results: Increased the density of activated catecholaminergic neurons in the ventral tegmental area but not in the locus coeruleus. Increased Fos expression in the medial preoptic area and arcuate nucleus of the hypothalamus, ventral tegmental area, locus coeruleus, and lateral paragigantocellular nucleus with chronic 22-day treatment. In vivo animal protocols: For brain activation studies, adult female Long Evans rats (225-250g) receive flibanserin hydrochloride (15 or 45 mg/kg) or vehicle by oral gavage twice daily for 22 days. Two hours after the final dose, rats are anesthetized and perfused transcardially with saline followed by 4% paraformaldehyde. Brains are removed, post-fixed, cryoprotected in 30% sucrose, and sectioned (30-40 microm). Fos expression (marker of neuronal activation) is detected by immunohistochemistry using anti-Fos antibody (1:1000) with DAB visualization. The number of Fos-positive neurons is quantified in brain regions including the medial preoptic area, arcuate nucleus, ventral tegmental area, and locus coeruleus by stereology. For microdialysis studies, guide cannulas are implanted in the prefrontal cortex of rats 5-7 days before experiments. |
| ADME/Pharmacokinetics |
Pharmacokinetics: In humans, flibanserin 100 mg (as the approved drug Addyi®) is administered orally once daily at bedtime due to somnolence side effects. After oral administration, Tmax is 0.5-1.5 hours, and bioavailability is low (~33%) due to extensive first-pass metabolism. Steady-state Cmax is approximately 500-1000 ng/mL. Flibanserin is highly protein-bound (>98%), primarily to albumin. The terminal elimination half-life (t1/2) is approximately 10-11 hours. Metabolism is primarily via CYP3A4-mediated oxidation, producing inactive metabolites including 6-hydroxy-flibanserin and flibanserin N-oxide. Excretion occurs in urine (44%) and feces (48%), mostly as metabolites. No significant accumulation occurs with daily dosing. Alcohol co-administration is contraindicated due to increased hypotension risk. In rats, flibanserin crosses the blood-brain barrier with brain:plasma ratio of 2-5.
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| Toxicity/Toxicokinetics |
Toxicology: Preclinical and clinical studies have established the safety profile. In rats, acute oral LD50 >2000 mg/kg. In repeat-dose studies (up to 26 weeks), NOAEL (No Observed Adverse Effect Level) is 25-50 mg/kg/day. In humans, the most common adverse events (≥10%) in clinical trials are somnolence (drowsiness), dizziness, nausea, and fatigue. Somnolence occurs in approximately 30% of patients, leading to the bedtime dosing recommendation. Serious adverse events are rare. Hypotension and syncope (fainting) may occur, especially when taken with alcohol, leading to a Boxed Warning for alcohol contraindication. No genotoxicity or carcinogenicity concerns identified. The FDA approved flibanserin for HSDD in premenopausal women in 2015 (Addyi®). Pregnancy category: Not recommended during pregnancy (limited data). The compound has a favorable safety profile when used as directed.
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| References |
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| Additional Infomation |
Flibanserin hydrochloride (propan-2-ol) hydrate is the active pharmaceutical ingredient (API) form of flibanserin, approved by the FDA in 2015 for the treatment of hypoactive sexual desire disorder (HSDD) in premenopausal women (brand name Addyi®). It is the first and only FDA-approved medication for this indication. The mechanism involves balancing serotonin and dopamine/norepinephrine neurotransmission in brain regions controlling sexual motivation and reward. The unique bedtime dosing schedule minimizes daytime somnolence. Flibanserin has also been investigated for depression, anxiety, and post-traumatic stress disorder but was not approved for these indications. The patent protection has expired, and generic versions are available. The compound is not scheduled as a controlled substance. Research continues on biomarkers to predict treatment response. For laboratory research, the compound is commercially available as a reference standard for analytical and pharmacological studies.
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| Molecular Formula |
C20H22CLF3N4O.0.5C3H8O.0.5H2O
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| Molecular Weight |
465.20
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| Appearance |
Solid powder
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| Synonyms |
BIMT-17 hydrochloride (propan-2-ol) hydrate; BIMT-17BS hydrochloride (propan-2-ol) hydrate
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| 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 | 2.1496 mL | 10.7481 mL | 21.4961 mL | |
| 5 mM | 0.4299 mL | 2.1496 mL | 4.2992 mL | |
| 10 mM | 0.2150 mL | 1.0748 mL | 2.1496 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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