Cat. No.: HY-15791

FR173657

Name: FR173657
Brand: MedChemExpress
SKU: HY-15791
Price: 900.00 USD
Availability: InStock
Rating: 5 (1 reviews)

(Synonyms: FK-3657)

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FR173657 (FK-3657) is an orally active, selective bradykinin B2 receptor antagonist. FR173657 induces Apoptosis, G0/G1 phase arrest, and p38 MAPK/p27Kip1 signaling. FR173657 blocks afferent neuron activation, tumor vascular hyperpermeability, tumor angiogenesis/growth, colorectal proliferation, kinin-mediated invasion/migration, and airway plasma extravasation. FR173657 can be used in research on inflammatory pain, asthma, triple-negative breast cancer, psoriasis, pancreatitis, acute cystitis, skin inflammation, sarcoma 180, colorectal liver metastasis, and Carrageenan-induced pleurisy.

For research use only. We do not sell to patients.

Purity : 99.00%
CAS No.: 167838-64-4
Formula: C₃₀H₂₇Cl₂N₅O₄
Molecular Weight:592.47

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

FR173657 Chemical Structure

CAS No.: 167838-64-4

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Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]

Bradykinin B2 Receptor (B2R)

All Bradykinin Receptor Isoforms :

All p38 MAPK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
IMR-90	IC50	2.9 nM	Displacement of [3H]-bradykinin binding to B2 receptors in human foetal lung fibroblast IMR-90 cells after 90 min incubation at room temperature measured by cell-based radioligand binding assay. Displacement of [3H]-bradykinin binding to B2 receptors in human foetal lung fibroblast IMR-90 cells after 90 min incubation at room temperature measured by cell-based radioligand binding assay.	9051299
MDA-MB-231	IC50	20 μM	Antiproliferative activity against human MDA-MB-231 cells assessed as viability reduction after 72 hrs by MTT assay. Antiproliferative activity against human MDA-MB-231 cells assessed as viability reduction after 72 hrs by MTT assay.	29515778

In Vitro

FR173657 (10 μM; 48 h) reduces the proliferation of MoCR and SW480 colorectal cancer cells^[3].
FR173657 (10 μM; 21 h) combined with BK reduces MoCR cell invasion by more than 90%^[3].
FR173657 (10 μM; 1 week) inhibits the anchorage-independent growth of MDA-MB-231 cells^[6].
FR173657 (10 μM; 0-360 min) activates p38 MAPK in MDA-MB-231 cells over time^[6].
The cytostatic activity of FR173657 is attenuated in B2R-knockdown MDA-MB-231 cells^[6].
FR173657 (0.1 nM-32 nM; 60 min) is a potent displacer of [³H]-BK binding at the B2 receptor in guinea pig ileum, with an IC₅₀ of 0.56 nM^[1].
FR173657 (0.01 nM-0.1 μM; 60 min) displaces [³H]-BK binding at rat uterine B2 receptors with an IC₅₀ of 1.5 nM^[1].
FR173657 (1 nM-10 nM; 10 min) is a potent and selective B2 antagonist in guinea pig isolated ileum that antagonizes BK-induced contraction, with an IC₅₀ of 7.9 nM and a pA2 of 9.2^[1].
FR173657 binds to hB2R in HEK-293T cells with an IC₅₀ of 37.0 nM^[6].
FR173657 (10 μM; 72 h) does not induce senescence in MDA-MB-231 cells^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[3]

Cell Line:

human SW480 and mouse MoCR colorectal cancer cell lines
Concentration:

10 μM; with or without BK
Incubation Time:

48 h
Result:

Significantly reduced proliferation in both MoCR and SW480 cells.
The reduction in proliferation was the same whether the B2R agonist BK was present or absent.

Cell Invasion Assay^[3]

Cell Line:

mouse MoCR colorectal cancer cells
Concentration:

10 μM; with BK
Incubation Time:

21 h
Result:

Resulted in over 90% reduction of invasion in MoCR cells when combined with BK.
BK did not restore invasion compared to controls.

In Vivo

FR173657 (6.8 mg/kg (ED₅₀ at 2 h); oral) inhibits Carrageenin-induced paw edema in rats^[1].
FR173657 (15 mg/kg; oral gavage; twice daily; from day 1 to day 21 after tumor induction) reduces tumor angiogenesis by 39% in CBA mice with CRLM, but does not significantly reduce tumor burden, percentage of viable tumor, or apoptosis^[3].
FR173657 (30 mg/kg; oral; once daily; days 7-12) inhibits late-stage tumor angiogenesis in S-180 tumor-bearing mice^[2].
FR173657 (30 mg/kg; oral; once daily; days 1-6, days 7-12, and days 1-12) reduces VEGF immunoreactivity in the tumor stroma of S-180 tumor-bearing mice^[2].
FR173657 (30 mg/kg; oral) blocks bradykinin-induced hypotension in conscious rats for at least 5 h without affecting basal MABP^[9].
FR173657 (3-30 mg/kg; intraperitoneal injection; once daily; six consecutive days) alleviates imiquimod-induced psoriasis-like skin inflammation in C57BL/6 mice, reducing PASI scores, keratinocyte proliferation and differentiation markers, immune cell infiltration (including neutrophils, macrophages, CD3⁺/CD4⁺/CD8⁺ T cells), IL-17, γδ T cells, lymphoid organ weight, and improving nesting behavior^[8].
FR173657 (15 mg/kg; p.o.; twice, 2 h apart) inhibits tumor vascular hyperpermeability in S-180 tumor-bearing mice, with the most significant effect at the early stage^[2].
FR173657 (5-20 mg/kg; oral) dose-dependently reduces bradykinin-induced plasma extravasation in the guinea pig trachea and main bronchi, completely eliminating it at 20 mg/kg^[5].
FR173657 (5-20 mg/kg; oral) dose-dependently inhibits antigen-induced plasma extravasation in the trachea and main bronchi of sensitized guinea pigs^[5].
FR173657 (30-300 nmol/kg; subcutaneous injection; 50-500 nmol/kg; oral; 1 h before induction) inhibits Caerulein (HY-A0190)-induced pancreatic edema and pancreatic tissue lipase retention in rats, with subcutaneous administration being effective from 30 nmol/kg, and oral administration also being active but with lower potency^[10].
FR173657 (0.075 mg/kg (ED₅₀); oral) inhibits BK-induced bronchoconstriction in guinea pigs^[1].
FR173657 (1 mg/kg; oral) does not inhibit histamine-induced bronchoconstriction in guinea pigs^[1].
FR173657 (0.3-3 µmol/kg; subcutaneous injection; 60 min before the experiment; 0.5-5.0 µmol/kg; oral administration) inhibits bradykinin-induced nociceptive behavioral responses in rats after both subcutaneous injection and oral administration, and the higher subcutaneous doses completely eliminate these responses^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Hartley (male)^[1]
Dosage:

1 mg/kg
Administration:

oral; after last histamine-induced bronchoconstriction
Result:

Did not inhibit histamine-induced increases in PIP even at 1 mg/kg; % inhibition was 6.2 (n=5).

Animal Model:

ICR (male, 5-week-old)^[2]
Dosage:

15 mg/kg per administration (reported as 30 mg/kg/day total)
Administration:

p.o.; twice, 2 h apart
Result:

Produced about 60% inhibition of tumor vascular permeability in the early phase (day 5).
Reduced vascular permeability in the late phase (day 10), but the extent of inhibition was much less than that seen in the early phase.
Suppressed vascular permeability at 30 mg/kg/day.

Animal Model:

ICR (male, 5-week-old)^[2]
Dosage:

30 mg/kg
Administration:

p.o.; once daily; days 1-6
Result:

Suppressed angiogenesis and tumor growth in the early phase at 30 mg/kg/day on days 1-6.

Animal Model:

ICR (male, 5-week-old)^[2]
Dosage:

30 mg/kg
Administration:

p.o.; once daily; days 7-12
Result:

Inhibited angiogenesis in the late phase at 30 mg/kg/day on days 7-12.
The relative inhibition was less than that produced by anti-VEGF neutralizing antibody.

Animal Model:

ICR (male, 5-week-old)^[2]
Dosage:

30 mg/kg
Administration:

p.o.; once daily; days 1-6, days 7-12, and days 1-12
Result:

Immunoreactive VEGF in tumor stromata was markedly reduced (30 mg/kg/day once daily on days 1-6, days 7-12, and days 1-12).

Animal Model:

CBA (male, 6-8 weeks old, body weight 24-28 g)^[3]
Dosage:

15 mg/kg twice daily (total 30 mg/kg/day)
Administration:

oral gavage; twice daily; starting day 1 post tumor induction until day 21
Result:

Reduced tumor load and tumor volume compared with control, but reductions were not significant.
The percentage of viable tumor was not reduced compared with control.
Did not increase tumor apoptosis compared with control.
Significantly reduced tumor angiogenesis, with a 39% reduction in vessel density compared to control.

Animal Model:

Sprague-Dawley (female)^[4]
Dosage:

s.c. 300 nmol kg−1 or 3 µmol kg−1; p.o. 0.5, 1.5, or 5.0 µmol kg−1
Administration:

s.c.; 60 min before experiment; p.o.; after overnight fasting
Result:

s.c. 300 nmol kg−1 caused partial inhibition of nociceptive behavioural responses; no score 3 licking or biting occurred (n = 6), and score 1 or 2 responses lasted 486 s (n = 6), observed only during the initial 10 min.
s.c. 3 µmol kg−1 abolished the nociceptive responses altogether.
p.o. 5 µmol kg−1 almost abolished the bradykinin-induced behavioural effects.
p.o. 1.5 µmol kg−1 strongly reduced the effects in 4 out of 8 animals, while the remaining 4 rats showed virtually no effect.
p.o. 0.5 µmol kg−1 was completely ineffective.

Animal Model:

Sprague-Dawley (female; 200-300 g)^[4]
Dosage:

s.c. 0.3-10 µmol kg−1 (lowest tested dose 300 nmol kg−1; higher doses 1-3 µmol kg−1; highest dose 10 µmol kg−1)
Administration:

s.c.; after third bradykinin challenge; bradykinin challenges continued for 90 min
Result:

s.c. inhibited bradykinin-induced hypotensive reflex responses in a dose-dependent manner.
The lowest dose, 300 nmol kg−1, had no effect, while higher doses, 1-3 µmol kg−1, caused a decrease in the responses to bradykinin.
The effect developed over a period of at least 60 min.
The ID50 was 1.1 µmol kg−1 (95% confidence interval 0.2-6.0 µmol kg−1).
The hydrochloric acid-induced hypotensive reflex was unchanged 90 min after administration of 10 µmol kg−1 (731 mmHg; n = 5).

Animal Model:

Hartley (male, 300-500 g)^[5]
Dosage:

5, 10, and 20 mg/kg
Administration:

p.o.; 30 min before bradykinin aerosol
Result:

In the trachea, reduced bradykinin-induced Evans blue extravasation to 70.0, 65.9, and 46.8 ng/mg wet weight (n=5 each).
In the main bronchi, reduced extravasation to 56.2, 47.8, and 34.3 ng/mg wet weight (n=5 each).
Abolished the bradykinin-induced increase in the trachea and main bronchi.

Animal Model:

Hartley (male, 300-500 g)^[5]
Dosage:

5, 10, and 20 mg/kg
Administration:

p.o.; 30 min before ovalbumin aerosol
Result:

In the trachea, produced Evans blue extravasation values of 83.3, 68.9, and 54.8 ng/mg wet weight (n=5 each).
In the main bronchi, produced values of 89.1, 71.7, and 60.1 ng/mg wet weight (n=5 each).
Inhibited ovalbumin-induced plasma extravasation by 77% in the trachea and 65% in the main bronchi.

Animal Model:

Hartley (male, 300-500 g)^[5]
Dosage:

20 mg/kg
Administration:

p.o.; 30 min before capsaicin aerosol
Result:

In the trachea, yielded 59.5 ng/mg wet weight (n=5).
In the main bronchi, yielded 83.3 ng/mg wet weight (n=5).
Did not affect capsaicin-induced plasma extravasation.

Animal Model:

C57BL/6 wild-type (WT; RRID: MGI:5656552; adult male and female, 8-10 weeks old, 20-25 g)^[8]
Dosage:

3 mg/kg, 10 mg/kg, and 30 mg/kg; 30 mg/kg (selected experiments)
Administration:

i.p.; once daily 30 min before imiquimod; six consecutive days
Result:

PASI scores were lower at all doses evaluated compared with the vehicle group.
Mice presented lower cellular infiltration and reduced imiquimod-induced hyperplasia.
At 10 and 30 mg/kg, the number of PCNA-staining keratinocytes was reduced compared with the vehicle group.
At 10 and 30 mg/kg, K14-labelled keratinocytes were decreased compared with the vehicle group.
At 30 mg/kg, Ly6G+ neutrophil accumulation was reduced compared with the vehicle group.
Skin macrophages were depleted and CD11b+ cell accumulation was reduced compared with the vehicle group.
The number of CD3+ T cells was reduced compared with the vehicle group.
The number of CD4+ infiltrating cells in imiquimod-induced psoriatic lesions was also reduced compared with the vehicle group.
The number of CD8+ T cells was diminished compared with the vehicle group.
IL-17 detected in imiquimod psoriatic lesions was decreased compared with the vehicle group.
The γδ T cell subset was reduced in the imiquimod-induced mouse model.
At 30 mg/kg, spleen weight was reduced and a protective effect on axillary and inguinal lymph node weights was shown compared with the vehicle group.
Mice displayed improved nest-building scores compared with the vehicle group.
The higher proliferation rates and faulty differentiation of keratinocytes induced by imiquimod were reduced.

Animal Model:

Sprague-Dawley (SD) (male, 8 weeks old, specific pathogen free)^[9]
Dosage:

30 mg/kg
Administration:

p.o.; single administration before i.v. BK/ACh challenges at 1, 2, 3, 5, and 7 h
Result:

Did not influence basal MABP throughout the experimental period.
Blocked BK-induced hypotensive responses by 95%, 91%, 90%, and 79% at 1, 2, 3, and 5 h after administration, respectively.
ACh-induced hypotension showed no marked changes over the 7 h experimental period.

Animal Model:

Sprague-Dawley (SD) (male, 8 weeks old, specific pathogen free)^[9]
Dosage:

3, 10, and 30 mg/kg; 30 mg/kg (duration testing)
Administration:

p.o.; 1 h before intrapleural BK; for duration, 1 to 7 h before BK
Result:

Intrapleural BK (0.3-10 nmol per rat) caused plasma exudation in a dose-dependent manner.
This exudation was inhibited by 85-97%.
Plasma exudation induced by BK 3 nmol per rat was inhibited, with the maximum effect obtained at 30 mg/kg.
The inhibitory effect persisted for at least 4 h; thereafter, 7 h after BK, the inhibitory effect on plasma exudation became incomplete.

Animal Model:

Sprague-Dawley (SD) (male, 8 weeks old, specific pathogen free)^[9]
Dosage:

30 mg/kg
Administration:

p.o.; 1 h before intrapleural histamine
Result:

Plasma exudation induced by intrapleural histamine (1 mmol per rat) was not affected.

Animal Model:

Sprague-Dawley (SD) (male, 8 weeks old, specific pathogen free)^[9]
Dosage:

30 mg/kg; 3 and 10 mg/kg
Administration:

p.o.; 1 h before carrageenin; repeated 3.5 h after carrageenin for 30 mg/kg; additional doses before carrageenin
Result:

Reduced the volume of exudate 3, 5, and 7 h after carrageenin by 41%, 47%, and 57%, respectively.
With 3 and 10 mg/kg, p.o., the volume of exudate 3 h after carrageenin was 0.70 mL (n=4) and 0.55 mL (n=4), respectively; the effect of the higher dose (10 mg/kg) was statistically significant.
Reduced plasma exudation rates 1, 3, 5, and 7 h after carrageenin by 52%, 53%, 76%, and 67%, respectively.
With 3 and 10 mg/kg, p.o., plasma exudation rates 3 h after carrageenin were 96 mg 20 min^-1 (n=4) and 73 mg 20 min^-1 (n=4), respectively; the effect of the higher dose (10 mg/kg) was statistically significant.
Did not affect plasma HMW or LMW kininogens in rats with carrageenin-induced pleurisy.
Did not affect intrapleural kininogen levels, and HMW kininogen levels were very low in rats.
Reduced intrapleural levels of BK-(1-5) by 59%.

Animal Model:

Sprague-Dawley (SD) (male, 8 weeks old, specific pathogen free)^[9]
Dosage:

30 mg/kg
Administration:

p.o.; 1 h before intrapleural compound 48/80
Result:

Compound 48/80 caused obvious plasma exudation at 20 min.
Did not reduce the plasma exudation at all in this model.

Animal Model:

Sprague-Dawley (female, 200-250 g)^[10]
Dosage:

10 nmol/kg; 30-300 nmol/kg (s.c.); 50 nmol/kg and above; 500 nmol/kg (p.o.)
Administration:

s.c. in DMSO, 0.5 mL/kg; p.o. intragastrically in 0.5% methylcellulose, 1 mL/kg; given 1 h before induction
Result:

Inhibited pancreatic oedema formation dose-dependently after s.c. injection at 30-300 nmol/kg; 10 nmol/kg was ineffective.
After p.o. administration, attenuated oedema at 50 nmol/kg and above; the maximum effect at the highest oral dose (500 nmol/kg) inhibited oedema by about 60%.
The difference between equieffective s.c. and p.o. doses was 0.8-1.2 log units.
Caused dose-dependent reduction of lipase accumulation in pancreatic tissue at s.c. 30-300 nmol/kg.
Also induced dose-dependent increases of lipase activity in blood serum due to improved removal of the enzyme from tissue.

Related Protocols :

Chemical Information

CAS No. 167838-64-4
Appearance Solid
Molecular Weight 592.47
Formula C₃₀H₂₇Cl₂N₅O₄
Color White to off-white
SMILES

O=C(NCC(N(C1=CC=C(Cl)C(COC2=C3N=C(C)C=CC3=CC=C2)=C1Cl)C)=O)/C=C/C4=CC=C(NC(C)=O)N=C4
Synonyms

FK-3657
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : 33.33 mg/mL (56.26 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.6878 mL

8.4392 mL

16.8785 mL

5 mM

0.3376 mL

1.6878 mL

3.3757 mL

10 mM

0.1688 mL

0.8439 mL

1.6878 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Dilution Calculator

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 3.33 mg/mL (5.62 mM); Clear solution

This protocol yields a clear solution of ≥ 3.33 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (33.3 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 3.33 mg/mL (5.62 mM); Clear solution

This protocol yields a clear solution of ≥ 3.33 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (33.3 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%
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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (303 KB)
SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Asano M, et al. The identification of an orally active, nonpeptide bradykinin B2 receptor antagonist, FR173657. British journal of pharmacology. 1997 Feb;120(4):617-24. [Content Brief]

[2]. Ishihara K, et al. Roles of bradykinin in vascular permeability and angiogenesis in solid tumor. International immunopharmacology. 2002 Mar;2(4):499-509.

[3]. da Costa PLN, et al. The kallikrein-Kinin system modulates the progression of colorectal liver metastases in a mouse model. BMC cancer. 2018 Apr 04;18(1):382.

[4]. Griesbacher T, et al. The nonpeptide B2 receptor antagonist FR173657: inhibition of effects of bradykinin related to its role in nociception. British journal of pharmacology. 1998 Jul;124(6):1328-34.

[5]. Watanabe M, et al. Effects of the orally active non-peptide bradykinin B2 receptor antagonist, FR173657, on plasma extravasation in guinea pig airways. European journal of pharmacology. 1999 Feb 19;367(2-3):373-8.

[6]. Dubuc C, et al. Targeting intracellular B2 receptors using novel cell-penetrating antagonists to arrest growth and induce apoptosis in human triple-negative breast cancer. Oncotarget. 2018 Feb 09;9(11):9885-9906.

[7]. Lesage A, et al. In vitro pharmacological profile of a new small molecule bradykinin B2 receptor antagonist. Frontiers in Pharmacology. 2020 Jun 19;11:916. [Content Brief]

[8]. Soley BDS, et al. B and B kinin receptor blockade improves psoriasis-like disease. British journal of pharmacology. 2020 Aug;177(15):3535-3551.

[9]. Majima M, et al. Effects of an orally active non-peptide bradykinin B2 receptor antagonist, FR173657, on plasma exudation in rat carrageenin-induced pleurisy. British journal of pharmacology. 1997 Jun;121(4):723-30.

[10]. Griesbacher T, et al. Effects of the non-peptide B2 receptor antagonist FR173657 in models of visceral and cutaneous inflammation. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2000 Oct;49(10):535-40.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.6878 mL	8.4392 mL	16.8785 mL	42.1962 mL
	5 mM	0.3376 mL	1.6878 mL	3.3757 mL	8.4392 mL
	10 mM	0.1688 mL	0.8439 mL	1.6878 mL	4.2196 mL
	15 mM	0.1125 mL	0.5626 mL	1.1252 mL	2.8131 mL
	20 mM	0.0844 mL	0.4220 mL	0.8439 mL	2.1098 mL
	25 mM	0.0675 mL	0.3376 mL	0.6751 mL	1.6878 mL
	30 mM	0.0563 mL	0.2813 mL	0.5626 mL	1.4065 mL
	40 mM	0.0422 mL	0.2110 mL	0.4220 mL	1.0549 mL
	50 mM	0.0338 mL	0.1688 mL	0.3376 mL	0.8439 mL

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FR173657

All Bradykinin Receptor Isoforms

All p38 MAPK Isoforms