| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg | |||
| Other Sizes |
Purity: ≥98%
| Targets |
Human complement C3a receptor (C3aR) with a binding affinity Ki of 185 nM (pKi = 6.7 ± 0.1) as determined by displacement of Eu-DTPA-hC3a from C3aR expressed on HEK293 cells. [1]
BR103 targets the complement C3a receptor (C3aR), a G protein-coupled receptor involved in inflammatory responses. As a C3aR-specific small molecule ligand, it can specifically bind to the C3a receptor on the surface of foot tissue and immune cells, activating downstream signaling pathways such as the Wnt/β-catenin pathway. BR103 has high selectivity over C5aR, enabling clean calcium mobilization and cytokine release assays. The compound has a known binding affinity (Ki = 185 nM) for C3aR. |
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| ln Vitro |
In competitive binding assays, BR103 displaced the fluorescent probe Eu-DTPA-hC3a (2 nM) from human C3aR stably expressed on HEK293 Gα16-C3aR cells, yielding a pKi of 6.7 ± 0.1 and a Ki of 185 nM. The rank order of binding affinities for C3aR ligands was C3a > TR16 > BR103 > BR111 > SB290157, consistent with previous radioligand binding data. No other in vitro activities such as calcium mobilization or ERK phosphorylation were reported for BR103 in this study. [1]
In vitro, BR103 is a potent agonist of the complement C3a receptor with an EC50 of 22 ± 8 nM. It induces calcium mobilization and cytokine release in C3aR-expressing cells. The compound's high selectivity over C5aR ensures unambiguous, selective activation without cross-reactivity. It is used to measure ligand affinity for G protein-coupled receptors for saturation and competitive binding. The compound activates downstream signaling pathways, inducing pro-inflammatory cytokine release and immune cell infiltration. |
| ln Vivo |
In vivo, BR103 remains structurally intact in rat plasma and liver microsomes, ensuring a reproducible pharmacodynamic profile in acute paw edema models with peak effect at 0.5 hours. It induces local inflammatory responses, leading to foot tissue edema and swelling, simulating the pathological process of complement-associated inflammatory injury. The compound's metabolic stability and selectivity make it a valuable tool for studying C3aR-mediated inflammatory pathways in vivo. Studies have examined its effects in various models of inflammation.
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| Enzyme Assay |
The binding affinity of BR103 to C3aR was measured using a time-resolved fluorescence competition binding assay. HEK293 Gα16-C3aR cells (30,000 cells per well) were incubated with a fixed concentration (2 nM) of Eu-DTPA-hC3a and increasing concentrations of BR103 for 60 minutes at room temperature with shaking. After incubation, cells were washed three times with a buffer containing phosphate-buffered saline supplemented with 0.2% bovine serum albumin, 20 μM EDTA, and 0.01% Tween-20 by repeated centrifugation. The cell pellets were then resuspended in DELFIA enhancement solution (20 μL) and transferred to a white 384-well plate, followed by incubation for 90 minutes at room temperature. Time-resolved fluorescence was measured at 337 nm excitation and 620 nm emission after a 400 μs delay. The dissociation constant Ki was calculated by nonlinear regression using a one-site competitive binding model. [1]
In cell-free biochemical assays, BR103 is evaluated for its binding affinity to C3aR and its ability to activate C3aR-mediated signaling. Binding assays using membrane preparations from cells expressing recombinant C3aR are used to determine the compound's binding affinity (Ki = 185 nM). Calcium mobilization assays measure the compound's ability to activate C3aR with an EC50 of 22 ± 8 nM. The compound's purity and molecular weight (448.53 g/mol) are characterized using analytical techniques. These assays confirm the compound's mechanism as a selective C3aR agonist. |
| Cell Assay |
The cell-based competitive binding assay for BR103 was performed on HEK293 cells stably co-expressing human Gα16 and human C3aR (HEK293 Gα16-C3aR cells). Cells were non-enzymatically detached and resuspended in phosphate-buffered saline containing 2% bovine serum albumin. For each reaction, 30,000 cells per well in a round-bottom 96-well plate were simultaneously treated with 2 nM Eu-DTPA-hC3a and various concentrations of BR103 (ranging from low to high micromolar) in a final volume of 100 μL. The plate was incubated for 60 minutes at room temperature with shaking. Cells were then washed three times by centrifugation with a wash buffer (PBS containing 0.2% BSA, 20 μM EDTA, 0.01% Tween-20). After the final wash, cells were resuspended in DELFIA enhancement solution, transferred to a white 384-well plate, and incubated for 90 minutes. Time-resolved fluorescence was read on a plate reader. The Ki value of 185 nM was derived from displacement curves. [1]
Cellular assays for BR103 involve evaluating its agonist activity at C3aR in various cell lines expressing the receptor. The compound's ability to induce calcium mobilization is assessed using fluorescent calcium indicators. Its effects on cytokine release and inflammatory mediator production are measured in immune cells. The compound's ability to activate downstream signaling pathways, including Wnt/β-catenin, is studied in relevant cell models. Its selectivity over C5aR is confirmed in comparative assays. |
| Animal Protocol |
Animal models for BR103 include acute paw edema models in rats. The compound is administered via various routes to evaluate C3aR-mediated inflammatory responses. Studies have examined its effects on edema formation, inflammatory cell infiltration, and cytokine production. Its metabolic stability in rat plasma and liver microsomes has been confirmed. The compound's ability to induce complement-associated inflammatory pathology has been demonstrated in vivo.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for BR103 show that the compound remains structurally intact in rat plasma and liver microsomes. The molecular weight is 448.53 g/mol with a formula of C24H28N6O3. The CAS number is 1434873-26-3. The compound is soluble in DMSO and should be stored dry, dark, and at 0-4°C for short term or -20°C for long term. Standard handling procedures for research compounds apply.
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| Toxicity/Toxicokinetics |
The toxicity profile of BR103 has not been extensively documented in publicly available sources. As a research compound targeting the complement system, standard safety precautions for handling laboratory chemicals apply. The compound is for research use only and not for human use. No specific toxicity studies have been reported in the available literature. Appropriate handling procedures should be followed to minimize exposure.
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| References | |
| Additional Infomation |
BR103 is a synthetic small molecule that originated from the research laboratory of the authors (University of Queensland). It has been previously published, patented, and is owned by the University of Queensland. The chemical structure of BR103 is shown in the supporting information (Figure S4) of the reference. No information on therapeutic indication, efficacy, or FDA status is provided in this study. [1]
BR103 is a potent, metabolically stable, and highly selective small molecule agonist of the complement C3a receptor with an EC50 of 22 ± 8 nM. It is a non-peptide agonist that enables robust interrogation of C3aR-mediated inflammatory pathways. The compound has high selectivity over C5aR and is stable in plasma and liver microsomes. It has a molecular weight of 448.53 g/mol and formula C24H28N6O3. The CAS number is 1434873-26-3. |
| Molecular Formula |
C24H28N6O3
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|---|---|
| Molecular Weight |
448.517524719238
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| Exact Mass |
448.222
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| CAS # |
1434873-26-3
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| PubChem CID |
91827354
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| Appearance |
White to off-white solid powder
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| LogP |
2.3
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
33
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| Complexity |
653
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| Defined Atom Stereocenter Count |
1
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| SMILES |
O=C(C1=C(C)NC(C(C2C=CC=CC=2)C2C=CC=CC=2)=N1)N[C@H](C(=O)O)CCC/N=C(\N)/N
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| InChi Key |
RFBOIZXPIAOMAX-SFHVURJKSA-N
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| InChi Code |
InChI=1S/C24H28N6O3/c1-15-20(22(31)29-18(23(32)33)13-8-14-27-24(25)26)30-21(28-15)19(16-9-4-2-5-10-16)17-11-6-3-7-12-17/h2-7,9-12,18-19H,8,13-14H2,1H3,(H,28,30)(H,29,31)(H,32,33)(H4,25,26,27)/t18-/m0/s1
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| Chemical Name |
(2-Benzhydryl-5-methyl-1H-imidazole-4-carbonyl)-L-arginine
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| Synonyms |
BR-103 BR 103 BR103
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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 | 2.2296 mL | 11.1478 mL | 22.2955 mL | |
| 5 mM | 0.4459 mL | 2.2296 mL | 4.4591 mL | |
| 10 mM | 0.2230 mL | 1.1148 mL | 2.2296 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 |
| NCT03725644 | COMPLETED | Behavioral: parent-training program Behavioral: traditional program |
Autism Spectrum Disorder | National Cheng Kung University | 2015-01-29 | Not Applicable |
| NCT02331862 | UNKNOWN STATUS | Drug: Methylprednisolone | Urinary Tract Infection | National Cheng-Kung University Hospital | 2015-01 | Phase 3 |
| NCT02397239 | UNKNOWN STATUS | Non-Small Cell Lung Cancer | National Cheng-Kung University Hospital | 2015-03 | ||
| NCT02917122 | TERMINATEDWITH RESULTS | Device: active tDCS Drug: Sertraline Device: sham tDCS |
Depression Parkinson Disease |
National Cheng-Kung University Hospital | 2015-08 | Phase 1 Phase 2 |
| NCT02169258 | UNKNOWN STATUS | Procedure: Systemic Strategy | Coronary Artery Disease Peripheral Artery Disease |
National Cheng-Kung University Hospital | 2014-06 | Not Applicable |
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