| Size | Price | Stock | Qty |
|---|---|---|---|
| 50mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| 500mg |
|
||
| 1g |
|
||
| 2g | |||
| Other Sizes |
Purity: ≥98%
Fexofenadine HCl (formerly MDL-16455A; Allegra; Terfenidine carboxylate; Telfast) is a potent histamine H1 receptor antagonist (antihistamine agent) used in the treatment of allergy symptoms such as hay fever, nasal congestion, and urticaria. Fexofenadine belongs to the second generation of antihistamines because, in contrast to first-generation antihistamines, it is less able to sedate people by crossing the blood-brain barrier.Fexofenadine has an IC50 value of 95.5 nM and demonstrates a strong, concentration-dependent anti-anaphylactic effect. For the 5-HT2A receptors from the rat caudal artery with a pA2 of 5.2, fexofenadine only exhibits a weak competitive antagonist behavior. On the P-gp-mediated secretion of Fexofenadine, verapamil's half-life (IC50) is 8.44 mM.
| Targets |
Histamine H1 receptor ( IC50 = 246 nM )
Histamine H1 receptor (H1R) (human H1R, Ki=0.36 nM; rat H1R, Ki=0.6 nM) [1,2] |
|---|---|
| ln Vitro |
In vitro activity: Fexofenadine has an IC50 value of 95.5 nM and demonstrates a strong, concentration-dependent anti-anaphylactic effect. For the 5-HT2A receptors from the rat caudal artery with a pA2 of 5.2, fexofenadine only exhibits a weak competitive antagonist behavior. On the Papp of fexofenadine in both directions in the Caco-2 cell model, all four P-gp inhibitors exhibit a strong, concentration-dependent effect.[1] On the P-gp-mediated secretion of Fexofenadine, verapamil's half-life (IC50) is 8.44 mM.[2] In the rabbit left ventricular wedge preparation, fed at doses greater than 100 times its free TPC, fedofenadine significantly increases the QT and Tp-e intervals and receives a significant TdP score.[3].
Radioligand binding assays with human H1R-expressing HEK293 cell membranes showed Fexofenadine HCl competitively bound to H1R with high affinity, displacing [3H]-pyrilamine in a concentration-dependent manner [2] - Human peripheral blood basophils stimulated with anti-IgE (1 μg/mL) were treated with Fexofenadine HCl (1 nM-10 μM). The drug dose-dependently inhibited histamine release, with maximum inhibition of 75% at 10 μM and IC50=0.8 μM [1] - Isolated guinea pig tracheal smooth muscle strips pre-contracted with histamine (1 μM) were treated with Fexofenadine HCl (0.1 μM-10 μM). It induced concentration-dependent relaxation, with EC50=1.3 μM, confirming H1R antagonistic activity [1] - Human atrial myocytes and ventricular cardiomyocytes were treated with Fexofenadine HCl (1 μM-100 μM). No significant effect on sodium, potassium, or calcium ion channel currents was observed, indicating no cardiotoxic potential [3] |
| ln Vivo |
Fexofenadine exhibits negligible metabolism in rats as evidenced by its unchanged excretion in urine, bile, and the gastrointestinal tract, rendering it a perfect probe for researching transport mechanisms. Coadministration of Fexofenadine with Ketoconazole increases the oral exposure of Fexofenadine by 187% in rats. On the other hand, rats given Fexofenadine in combination with either orange juice or apple juice experience a 31% or 22% reduction in oral exposure to the drug. Fexofenadine oral exposure is further reduced by increasing the amount of orange or apple juice given, by 40% and 28%, respectively.[4] The clearance of Fexofenadine from the biliary system (17 ml/min/kg) in mice makes up nearly 60% of the total clearance (30 ml/min/kg). Knockout mice of Mdr1a/1b P-gp does not affect the biliary excretion clearance with regard to both plasma and liver concentrations, whereas the absence of P-gp causes a 6-fold increase in the plasma concentration and 3-fold higher brain-to-plasma concentration ratio after oral administration.[5]
Passive cutaneous anaphylaxis (PCA) model in rats: Oral administration of Fexofenadine HCl (1 mg/kg, 3 mg/kg, 10 mg/kg) 1 hour before antigen challenge dose-dependently inhibited skin wheal formation, with 80% inhibition at 10 mg/kg [2] - Allergic rhinitis model in guinea pigs: Intranasal ovalbumin challenge induced sneezing and rhinorrhea. Oral Fexofenadine HCl (5 mg/kg/day) for 7 days reduced sneezing frequency by 68% and nasal secretion by 62% [1] - Clinical trial in patients with seasonal allergic rhinitis: Oral Fexofenadine HCl (180 mg/day) for 4 weeks improved nasal symptoms (sneezing, rhinorrhea, itching) by 72% and ocular symptoms by 65% compared to placebo. Symptom relief was sustained for 24 hours [1] - Cardiovascular safety study in dogs: Intravenous administration of Fexofenadine HCl (1 mg/kg-10 mg/kg) did not cause significant changes in heart rate, blood pressure, or QT interval, confirming cardiovascular safety [3] |
| Enzyme Assay |
H1R binding assay: Prepare membrane fractions from HEK293 cells expressing human H1R. Incubate membranes with [3H]-pyrilamine (0.5 nM) and various concentrations of Fexofenadine HCl (0.01 nM-100 nM) at 25°C for 60 minutes. Separate bound and free ligand by vacuum filtration through glass fiber filters. Measure radioactivity with a liquid scintillation counter and calculate Ki values using the Cheng-Prusoff equation [2]
|
| Cell Assay |
Fexofenadine hydrochloride (MDL-16455 hydrochloride) (100 µM; 1 hour) efficiently inhibits phosphorylated p38 activation in histamine-induced nasal fibroblasts.
Basophil histamine release assay: Isolate human peripheral blood basophils via density gradient centrifugation. Resuspend cells in buffer and pre-treat with Fexofenadine HCl (1 nM-10 μM) for 30 minutes. Stimulate with anti-IgE (1 μg/mL) for 60 minutes at 37°C. Centrifuge to collect supernatant and measure histamine concentration via fluorometric assay [1] - Tracheal smooth muscle relaxation assay: Isolate guinea pig tracheal strips, mount in organ baths with oxygenated Krebs-Ringer solution (37°C, 95% O2/5% CO2), and equilibrate for 60 minutes. Pre-contract with histamine (1 μM), then add Fexofenadine HCl (0.1 μM-10 μM) cumulatively and record tension changes [1] - Cardiomyocyte ion channel assay: Isolate human atrial and ventricular cardiomyocytes, seed on glass coverslips, and incubate for 24 hours. Treat with Fexofenadine HCl (1 μM-100 μM) for 30 minutes. Use whole-cell patch-clamp technique to record sodium, potassium, and calcium ion channel currents [3] |
| Animal Protocol |
C57BL/6 mice infected with Trichinella spiralis
5, 10 and 20 mg/kg Oral administration; 5, 10 and 20 mg/kg; once daily; 3 weeks PCA rat model: Male Wistar rats (150-200 g) were intradermally injected with anti-ovalbumin IgE (0.1 mL) on the back. After 48 hours, Fexofenadine HCl was dissolved in physiological saline and administered via oral gavage (1 mg/kg, 3 mg/kg, 10 mg/kg). One hour later, intravenous injection of ovalbumin (1 mg/kg) + Evans blue (5 mg/kg) was given. Thirty minutes later, rats were euthanized, and skin wheal area was measured [2] - Allergic rhinitis guinea pig model: Male Hartley guinea pigs (300-350 g) were sensitized with ovalbumin (100 μg) + aluminum hydroxide (2 mg) via intraperitoneal injection on days 0 and 7. From day 14, intranasal ovalbumin (1% solution) was administered once daily for 7 days. Fexofenadine HCl (5 mg/kg) was given via oral gavage once daily 1 hour before challenge. Record sneezing frequency and nasal secretion for 10 minutes post-challenge [1] - Canine cardiovascular safety model: Male beagle dogs (10-15 kg) were anesthetized with pentobarbital. A carotid artery catheter and jugular vein catheter were implanted to measure blood pressure and administer drugs. Fexofenadine HCl (1 mg/kg-10 mg/kg) was injected intravenously, and heart rate, blood pressure, and QT interval were recorded for 120 minutes post-administration [3] |
| ADME/Pharmacokinetics |
Absorption: Oral bioavailability is 35% (human); peak plasma concentration (Cmax) is reached 2-3 hours after oral administration (180 mg dose: Cmax = 310 ng/mL) [1]
- Distribution: Volume of distribution (Vd) is 5.4 L/kg (human); brain/plasma concentration ratio <0.01, indicating extremely low blood-brain barrier penetration [1] - Metabolism: Very little is metabolized in the liver (<5% of the dose), >90% is excreted unchanged [1,2] - Excretion: 60% of the dose is excreted in feces, and 40% is excreted in urine (both are excreted unchanged). Human elimination half-life (t1/2) is 14-18 hours [1] - Plasma protein binding rate: The plasma protein binding rate of fexofenadine hydrochloride in human plasma is 60-70% [1] |
| Toxicity/Toxicokinetics |
Acute toxicity: LD50 in rats and mice > 2000 mg/kg (oral); no deaths or serious clinical symptoms were reported [1] - Chronic toxicity: No significant hepatotoxicity or hematologic abnormalities were observed in rats after 6 months of oral administration of fexofenadine hydrochloride (100 mg/kg/day) [1] - Clinical side effects: Mild headache (4-6% of patients), fatigue (2-3%) and dry mouth (1-2%) have been reported. Due to the extremely low blood-brain barrier penetration, no sedative effects or cognitive impairment were observed [1] - Drug interactions: No significant interactions with CYP3A4 inhibitors (e.g., ketoconazole) or P-glycoprotein substrates; no effect on plasma concentrations of warfarin or digoxin [1,3]
|
| References | |
| Additional Infomation |
Fexofenadine hydrochloride is a diarylmethane compound. Fexofenadine hydrochloride is the hydrochloride salt form of fexofenadine, a carboxylated metabolic derivative of terfenadine. It belongs to the second-generation, long-acting, selective histamine H1 receptor antagonists and possesses antihistamine activity. After administration, fexofenadine competitively binds to peripheral H1 receptors in the gastrointestinal tract, blood vessels, and bronchial smooth muscle. This prevents histamine from binding to peripheral H1 receptors and inhibits their activation, thereby preventing histamine-mediated allergic reactions. Fexofenadine cannot cross the blood-brain barrier (BBB). See also: Fexofenadine (with active moiety)... See more...
Fexofenadine hydrochloride is a second-generation, non-sedating histamine H1 receptor antagonist with high selectivity for H1 receptors [1,2]. Its mechanism of action is competitive binding to H1R, blocking histamine-mediated allergic reactions (histamine release, vascular hyperpermeability, smooth muscle contraction)[1]. Indications include seasonal and perennial allergic rhinitis (relief of sneezing, runny nose, and nasal itching) and chronic idiopathic urticaria (relief of wheals and itching)[1]. It has no significant affinity for H2 receptors, muscarinic receptors, or adrenergic receptors, and it can hardly cross the blood-brain barrier. Avoid sedation and anticholinergic side effects[1,2]. It has a long elimination half-life (14-18 hours) and sustained efficacy, supporting once-daily dosing (180 mg) in adults[1]. |
| Molecular Formula |
C32H40CLNO4
|
|
|---|---|---|
| Molecular Weight |
538.12
|
|
| Exact Mass |
537.264
|
|
| Elemental Analysis |
C, 71.42; H, 7.49; Cl, 6.59; N, 2.60; O, 11.89
|
|
| CAS # |
153439-40-8
|
|
| Related CAS # |
Fexofenadine; 83799-24-0; Fexofenadine-d6; 548783-71-7; Fexofenadine-d10 hydrochloride; 1215821-44-5
|
|
| PubChem CID |
63002
|
|
| Appearance |
White to off-white solid powder
|
|
| Melting Point |
148-150oC
|
|
| LogP |
6.25
|
|
| Hydrogen Bond Donor Count |
4
|
|
| Hydrogen Bond Acceptor Count |
5
|
|
| Rotatable Bond Count |
10
|
|
| Heavy Atom Count |
38
|
|
| Complexity |
678
|
|
| Defined Atom Stereocenter Count |
0
|
|
| SMILES |
Cl[H].O([H])C(C1C([H])=C([H])C([H])=C([H])C=1[H])(C1C([H])=C([H])C([H])=C([H])C=1[H])C1([H])C([H])([H])C([H])([H])N(C([H])([H])C([H])([H])C([H])([H])C([H])(C2C([H])=C([H])C(=C([H])C=2[H])C(C(=O)O[H])(C([H])([H])[H])C([H])([H])[H])O[H])C([H])([H])C1([H])[H]
|
|
| InChi Key |
RRJFVPUCXDGFJB-UHFFFAOYSA-N
|
|
| InChi Code |
InChI=1S/C32H39NO4.ClH/c1-31(2,30(35)36)25-17-15-24(16-18-25)29(34)14-9-21-33-22-19-28(20-23-33)32(37,26-10-5-3-6-11-26)27-12-7-4-8-13-27;/h3-8,10-13,15-18,28-29,34,37H,9,14,19-23H2,1-2H3,(H,35,36);1H
|
|
| Chemical Name |
2-[4-[1-hydroxy-4-[4-[hydroxy(diphenyl)methyl]piperidin-1-yl]butyl]phenyl]-2-methylpropanoic acid;hydrochloride
|
|
| Synonyms |
|
|
| 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 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)
|
| Solubility (In Vitro) |
|
|||
|---|---|---|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.65 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 25.0 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: ≥ 2.5 mg/mL (4.65 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.8583 mL | 9.2916 mL | 18.5832 mL | |
| 5 mM | 0.3717 mL | 1.8583 mL | 3.7166 mL | |
| 10 mM | 0.1858 mL | 0.9292 mL | 1.8583 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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05720455 | Not yet recruiting | Drug: Fexofenadine HCL and pseudoephedrine HCL |
Rhinitis Allergic | Sanofi | July 21, 2024 | Phase 4 |
| NCT04534153 | Recruiting | Drug: Fexofenadine Hydrochloride without sodium lauryl sulfate Drug: Fexofenadine Hydrochloride with sodium lauryl sulfate |
The Impact of Excipients on Drug Absorption |
University of California, San Francisco |
January 31, 2023 | Early Phase 1 |
| NCT05264025 | Recruiting | Drug: Fexofenadine Drug: Placebo |
Rheumatoid Arthritis | October 6 University | October 2002 | Phase 1 Phase 2 |
| NCT04726345 | Recruiting | Drug: Fexofenadine Hcl 180Mg Tab Drug: Placebo |
Nephrolithiasis | Columbia University | June 29, 2021 | Phase 2 |
| NCT04688788 | Recruiting | Drug: Rituximab Drug: Ocrelizumab Drug: Fexofenadine |
Relapsing Remitting Multiple Sclerosis Primary Progressive Multiple Sclerosis |
Rigshospitalet, Denmark | April 28, 2021 | Phase 3 |
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA