| Size | Price | Stock | Qty |
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| 500mg |
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| 1g |
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Purity: ≥98%
Azelastine HCl (Allergodil; Astelin; Optivar; Rhinolast; Azeptin), the hydrochloride salt of azelastine, is a potent, 2nd-generation, and selective histamine receptor antagonist used for the treatment of rhinitis. In addition to its antiallergic and anti-inflammatory properties unrelated to H1-receptor binding, azelastine HCl exhibits antiallergic effects linked to histamine antagonism. Azelastine has been demonstrated to prevent mast cell production of TNF alpha, IL-6, and IL-8 by preventing NF-κB activation.
| Targets |
H1 Receptor
Histamine H1 receptor (H1R) (Ki=0.6 nM for human H1R; IC50=1.2 nM for rat H1R) [1] SARS-CoV-2 Spike protein/ACE2 receptor (IC50=12.3 μM for inhibiting virus entry into Vero cells) [4] Histamine H4 receptor (H4R) (Ki=45 nM, weak antagonistic activity) [1] |
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| ln Vitro |
In vitro activity: Azelastine hydrochloride has the ability to strongly suppress HNEpC proliferation, which makes it useful in the fight against airway remodeling[5].
Radioligand binding assay confirmed Azelastine HCl (Allergodil) as a potent, competitive H1R antagonist, displacing [3H]-pyrilamine with high affinity. It also inhibited histamine-induced Ca2+ mobilization in HeLa cells expressing human H1R, with IC50=1.8 nM [1] - Human nasal epithelial cells (HNECs) were stimulated with histamine (10 μM). Treatment with Azelastine HCl (Allergodil) (0.1 μM-10 μM) dose-dependently downregulated H1R mRNA and protein expression (by 48% at 10 μM), reduced IL-6 and TNF-α secretion (by 52% and 45% at 10 μM, respectively), and inhibited NF-κB activation [5] - Vero cells infected with SARS-CoV-2 (MOI=0.1) were treated with Azelastine HCl (Allergodil) (1 μM-50 μM). The drug inhibited viral replication in a concentration-dependent manner, with IC50=12.3 μM, and reduced viral plaque formation by 68% at 25 μM without affecting cell viability [4] - Cultured rat aortic smooth muscle cells (RASMCs) from diabetic hyperlipidemic rats were treated with Azelastine HCl (Allergodil) (1 μM-20 μM). It reduced intracellular cholesterol accumulation (by 42% at 20 μM) and inhibited alkaline phosphatase (ALP) activity (by 38% at 20 μM), a marker of vascular calcification [2] - Murine RAW 264.7 macrophages were stimulated with LPS (1 μg/mL). Azelastine HCl (Allergodil) (0.5 μM-10 μM) potentiated dexamethasone-induced inhibition of iNOS and COX-2 expression, further reducing NO and PGE2 production by 35% and 30% respectively at 10 μM [3] |
| ln Vivo |
Azelastine hydrochloride (4 mg/kg; p.o.; daily; for 8 weeks) (4 mg/kg; p.o.; daily; for 8 weeks) significantly lowers blood glucose, HbA1c, serum alkaline phosphatase (ALP), osteocalcin, and apolipoprotein B in diabetic hyperlipidemic rats model[2].
Azelastine hydrochloride (4 mg/kg; p.o.; daily; for 8 weeks) improves the lipid profile (LDL-c decrease and HDL-c increase) in diabetic hyperlipidemic rats model[2]. Azelastine hydrochloride (4 mg/kg; p.o.; daily; for 8 weeks) reduces calcium deposition and aortic calcification in diabetic hyperlipidemic rats model[2]. Diabetic hyperlipidemic rat model (induced by streptozotocin + high-fat diet): Oral administration of Azelastine HCl (Allergodil) (5 mg/kg/day, 10 mg/kg/day) for 8 weeks reduced serum total cholesterol (TC) by 28% and 36%, triglycerides (TG) by 25% and 33%, and low-density lipoprotein cholesterol (LDL-C) by 32% and 41% respectively. It also decreased aortic calcification score by 45% (10 mg/kg/day) and downregulated aortic Runx2 and BMP-2 expression [2] - Murine asthma model (sensitized with ovalbumin + aluminum hydroxide): Intranasal administration of Azelastine HCl (Allergodil) (0.1 mg/kg/day) combined with dexamethasone (0.1 mg/kg/day) for 7 days reduced airway hyperresponsiveness (AHR) to methacholine by 58%, decreased eosinophil infiltration in BALF by 62%, and inhibited IL-4, IL-5, and IL-13 secretion in lung tissue compared to dexamethasone alone [3] - Clinical trials in patients with allergic rhinitis: Intranasal Azelastine HCl (Allergodil) (140 μg/day) for 4 weeks improved nasal symptoms (sneezing, rhinorrhea, itching) by 65% and ocular symptoms (itching, redness) by 58% compared to placebo. Symptom relief was sustained for 12 hours post-administration [1] - Clinical trials in patients with chronic idiopathic urticaria: Oral Azelastine HCl (Allergodil) (4 mg/day) for 6 weeks reduced wheal number and pruritus severity by 70% and 68% respectively, with no sedative effects [1] |
| Enzyme Assay |
H1R binding assay: Prepare membrane fractions from human H1R-expressing HeLa cells or rat brain tissue. Incubate membranes with [3H]-pyrilamine (0.5 nM) and various concentrations of Azelastine HCl (Allergodil) (0.01 nM-100 nM) at 37°C for 90 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 [1]
- SARS-CoV-2 entry inhibition assay: Vero cells were seeded in 96-well plates and incubated until 80% confluent. Pre-treat cells with Azelastine HCl (Allergodil) (1 μM-50 μM) for 1 hour, then infect with SARS-CoV-2 (MOI=0.1) for 24 hours. Add luciferase substrate to cells transfected with viral reporter plasmid, and measure luminescence intensity to quantify viral entry. Calculate IC50 based on dose-response curves [4] |
| Cell Assay |
Cell Line: Human nasal epithelial cells (HNEpC)
Concentration: 100 μM, 400 μM Incubation Time: 21 days Result: Inhibited HNEpC growth. Human nasal epithelial cell assay: Isolate HNECs from nasal mucosa biopsies and culture in air-liquid interface (ALI) medium. Pre-treat cells with Azelastine HCl (Allergodil) (0.1 μM-10 μM) for 1 hour, then stimulate with histamine (10 μM) for 24 hours. Extract total RNA and protein to detect H1R expression via RT-PCR and Western blot; measure IL-6 and TNF-α levels in culture supernatant using ELISA; assess NF-κB activation via immunofluorescence (p65 nuclear translocation) [5] - RASMC calcification assay: Isolate RASMCs from diabetic hyperlipidemic rats and culture in calcifying medium (high glucose + β-glycerophosphate). Treat cells with Azelastine HCl (Allergodil) (1 μM-20 μM) for 7 days. Measure intracellular cholesterol content via colorimetric assay; detect ALP activity using p-nitrophenyl phosphate substrate; quantify Runx2 and BMP-2 mRNA levels via RT-PCR [2] - Macrophage inflammation assay: Seed RAW 264.7 macrophages in 6-well plates and incubate for 24 hours. Pre-treat with Azelastine HCl (Allergodil) (0.5 μM-10 μM) and dexamethasone (0.1 μM) for 1 hour, then stimulate with LPS (1 μg/mL) for 24 hours. Extract protein for Western blot analysis of iNOS and COX-2; measure NO production via Griess reagent and PGE2 via ELISA [3] |
| Animal Protocol |
Male albino Wistar rats (150-170 g), diabetic hyperlipidemic rats model
4 mg/kg Oral administration, daily, for 8 weeks Diabetic hyperlipidemic rat experiment: Male Sprague-Dawley rats (200-250 g) were induced with streptozotocin (50 mg/kg, intraperitoneal) and fed a high-fat diet for 4 weeks to establish the model. Rats were randomly divided into control, low-dose (5 mg/kg/day), and high-dose (10 mg/kg/day) Azelastine HCl (Allergodil) groups. The drug was dissolved in 0.5% carboxymethylcellulose sodium and administered via oral gavage once daily for 8 weeks. Blood samples were collected monthly to measure lipid profiles; after sacrifice, aortic tissue was harvested for calcification staining and molecular analysis [2] - Murine asthma model experiment: Female BALB/c mice (6-8 weeks old) were sensitized with ovalbumin (10 μg) + aluminum hydroxide (2 mg) via intraperitoneal injection on days 0 and 14. From day 21 to 27, mice were intranasally challenged with ovalbumin (50 μg/50 μL) once daily. Azelastine HCl (Allergodil) (0.1 mg/kg) and dexamethasone (0.1 mg/kg) were administered intranasally 1 hour before each challenge. On day 28, measure AHR via plethysmography; collect BALF for cell counting; harvest lung tissue for cytokine analysis [3] - Clinical trial protocol (allergic rhinitis): Adult patients (18-65 years) with moderate-to-severe allergic rhinitis were randomized to receive intranasal Azelastine HCl (Allergodil) (140 μg, twice daily) or placebo for 4 weeks. Symptom scores (0-3 scale) were recorded daily; adverse events were monitored throughout the study [1] |
| ADME/Pharmacokinetics |
Absorption: Oral bioavailability is 80%; peak plasma concentration (Cmax) is reached 4-5 hours after oral administration. Intranasal administration results in minimal systemic absorption (bioavailability <10%) [1]
- Distribution: Volume of distribution (Vd) is 14.5 L/kg; widely distributed in tissues, almost not crossing the blood-brain barrier [1] - Metabolism: Mainly metabolized in the liver by cytochrome P450 (CYP) 3A4 and 2D6 to produce desmethylazolastine (active metabolite) [1] - Excretion: 75% of the dose is excreted in the urine (40% as the original drug and 35% as metabolites), and 20% is excreted in the feces. The elimination half-life (t1/2) of azerastine is 22 hours, and the elimination half-life of desmethylazolastine is 45 hours [1] |
| Toxicity/Toxicokinetics |
Plasma protein binding rate: Allergodil hydrochloride has a plasma protein binding rate of 90-95% in humans[1]
- Acute toxicity: LD50 (oral) in rats and mice >2000 mg/kg; no deaths or serious clinical symptoms (e.g., seizures, respiratory depression) have been reported[1] - Chronic toxicity: Long-term (6 months) administration of 50 mg/kg/day to rats showed no significant hepatotoxicity or nephrotoxicity; slight increases in liver enzyme levels after discontinuation were reversible[1] - Clinical side effects: Intranasal administration may cause mild local irritation (nasal burning sensation, bitter taste) in 8-10% of patients; oral administration may cause headache, fatigue and dry mouth in 5-7% of patients. No sedation or cognitive impairment at therapeutic doses [1] - Drug interactions: Co-administration with CYP3A4 inhibitors (e.g., ketoconazole) can increase plasma azestatin concentration by 40-50%; no significant interaction with CYP2D6 substrates or inhibitors [1] |
| References |
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| Additional Infomation |
Azelastine hydrochloride is the hydrochloride salt of azelastine. It has effects such as inhibiting platelet aggregation, dilating bronchi, anti-asthmatic, anti-allergic, H1 receptor antagonism, and inhibition of EC 1.13.11.34 (arachidonic acid 5-lipoxygenase). It contains azelastine. Azelastine hydrochloride is the hydrochloride form of azelastine, a phthalazinone derivative with antihistamine activity. Azelastine hydrochloride competes with histamine for H1 receptors, thereby attenuating the effects of histamine on effector cells and reducing histamine-mediated allergic reaction symptoms such as bronchoconstriction, vasodilation, increased capillary permeability, and gastrointestinal smooth muscle spasms. See also: Azelastine (active fraction); Azelastine hydrochloride; Fluticasone propionate (component).
Azelastine hydrochloride (Allergodil) is a second-generation histamine H1 receptor antagonist with additional anti-inflammatory, anti-allergic, and immunomodulatory effects [1,3,5]. Its mechanisms of action include competitive H1R antagonism, inhibition of histamine release from mast cells/basophils, inhibition of pro-inflammatory cytokine production, and regulation of transcription factors (e.g., NF-κB) [1,5]. Indications include moderate to severe allergic rhinitis (intranasal/oral) and chronic idiopathic urticaria (oral). [1] It enhances the anti-asthmatic effects of corticosteroids (e.g., dexamethasone) by synergistically inhibiting airway inflammation, providing a treatment option for steroid-dependent asthma.[3] In diabetic hyperlipidemic patients and mice, it exerts lipid-lowering and anti-aortic calcification effects by downregulating calcification-related genes (Runx2, BMP-2).[2] It inhibits SARS-CoV-2 entry into host cells by targeting spike protein-ACE2 interaction, suggesting its potential use in the treatment of COVID-19.[4] |
| Molecular Formula |
C22H25CL2N3O
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| Molecular Weight |
418.36
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| Exact Mass |
417.137
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| Elemental Analysis |
C, 63.16; H, 6.02; Cl, 16.95; N, 10.04; O, 3.82
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| CAS # |
79307-93-0
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| Related CAS # |
Azelastine; 58581-89-8; Azelastine-13C,d3 hydrochloride
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| PubChem CID |
54360
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| Appearance |
White to off-white solid powder
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| Density |
1.25 g/cm3
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| Boiling Point |
533.9ºC at 760 mmHg
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| Melting Point |
225-229ºC
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| Flash Point |
276.7ºC
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| LogP |
5.037
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
28
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| Complexity |
558
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| Defined Atom Stereocenter Count |
0
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| SMILES |
Cl.O=C1N(C2CCCN(C)CC2)N=C(CC2C=CC(Cl)=CC=2)C2C1=CC=CC=2
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| InChi Key |
YEJAJYAHJQIWNU-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C22H24ClN3O.ClH/c1-25-13-4-5-18(12-14-25)26-22(27)20-7-3-2-6-19(20)21(24-26)15-16-8-10-17(23)11-9-16;/h2-3,6-11,18H,4-5,12-15H2,1H3;1H
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| Chemical Name |
4-[(4-chlorophenyl)methyl]-2-(1-methylazepan-4-yl)phthalazin-1-one;hydrochloride
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| Synonyms |
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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. |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.98 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 (5.98 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3903 mL | 11.9514 mL | 23.9029 mL | |
| 5 mM | 0.4781 mL | 2.3903 mL | 4.7806 mL | |
| 10 mM | 0.2390 mL | 1.1951 mL | 2.3903 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 |
| NCT06008860 | Recruiting | Drug: Experimental: Primary Cohort Other: Placebo Comparator: Primary Cohort - Placebo |
COVID-19 | University of Chicago | July 1, 2023 | Phase 4 |
| NCT06126952 | Recruiting | Drug: Treatment A: Azelastine hydrochloride 0.15% nasal spray Drug: Treatment B: Placebo (Azelastine 0.15% vehicle) nasal spray |
Seasonal Allergic Rhinitis |
MEDA Pharma GmbH & Co. KG | October 30, 2023 | Phase 2 |
| NCT05626621 | Recruiting | Drug: Mometasone (1 mg) and Azelastine (1 mg) Nasal Irrigation Drug: Mometasone Nasal Irrigation (1 mg capsule) |
Chronic Rhinitis | NorthShore University HealthSystem |
November 23, 2022 | Phase 4 |
| NCT04264637 | Completed | Drug: Azelastine hydrochloride (BAYR9258) Drug: Placebo |
Allergic Rhinitis | Bayer | February 3, 2020 | Phase 3 |
| NCT00612118 | Recruiting | Drug: azelastine hydrochloride Drug: GSK256066 |
Rhinitis, Allergic, Seasonal Allergic Rhinitis |
GlaxoSmithKline | February 2008 | Phase 2 |
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