| Identification | Back Directory | [Name]
1-benzyl-N-(furan-2-ylmethyl)benzimidazol-2-amine | [CAS]
831234-13-0 | [Synonyms]
AC1903
AC1903 >=98% (HPLC)
1-benzyl-N-(furan-2-ylmethyl)benzimidazol-2-amine
1-benzyl-N-(furan-2-ylmethyl)-1H-benzo[d]imidazol-2-amine
1H-Benzimidazol-2-amine, N-(2-furanylmethyl)-1-(phenylmethyl)- | [Molecular Formula]
C19H17N3O | [MDL Number]
MFCD06609959 | [MOL File]
831234-13-0.mol | [Molecular Weight]
303.36 |
| Chemical Properties | Back Directory | [Boiling point ]
512.4±60.0 °C(Predicted) | [density ]
1.20±0.1 g/cm3(Predicted) | [storage temp. ]
-20°C | [solubility ]
Soluble in DMSO (up to 30 mg/ml) or in Ethanol (up to 25 mg/ml) | [form ]
solid | [pka]
6.09±0.10(Predicted) | [color ]
Beige | [Stability:]
Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months. | [InChI]
InChI=1S/C19H17N3O/c1-2-7-15(8-3-1)14-22-18-11-5-4-10-17(18)21-19(22)20-13-16-9-6-12-23-16/h1-12H,13-14H2,(H,20,21) | [InChIKey]
OECUWHDVQIITIS-UHFFFAOYSA-N | [SMILES]
C1(NCC2=CC=CO2)N(CC2=CC=CC=C2)C2=CC=CC=C2N=1 |
| Hazard Information | Back Directory | [Description]
AC1903 is an inhibitor of transient receptor potential canonical channel 5 (TRPC5; IC50 = 14.7 μM). It is selective for TRPC5 over TRPC4 and TRPC6 at concentrations up to 100 and 30 μM, respectively. It inhibits TRPC5 in a concentration-dependent manner in HEK293 cells when used at concentrations ranging from 1 to 100 μM. AC1903 (30 μM) inhibits angiotensin II-induced production of reactive oxygen species (ROS) in wild-type podocytes and podocytes expressing a mutant angiotensin II type 1 (AT1) receptor that cannot be inactivated and endocytosed. It also suppresses proteinuria as well as reduces pseudocyst formation and podocyte loss in an AT1 receptor transgenic rat model of kidney disease when administered at a dose of 50 mg/kg twice per day. In a model of hypertension-induced focal segmental glomerulosclerosis (FSGS) using Dahl salt-sensitive rats, AC1903 decreases the rate of proteinuria when administered at the beginning of a high-salt diet and prevents progression when administered one week following initiation of a high-salt diet. | [Uses]
AC1903 is a TRPC5 inhibitor with valuable potential for the treatment of progressive kidney diseases. AC1903 inhibits TRPC5 ion channels and suppresses progressive kidney diseases via TRPC5-AT1R related genetic pathways. ?AC1903 also provides therapeutic benefit in a rat model of hypertensive proteinuric kidney disease. | [in vivo]
AC1903 (intraperitoneal injection; 50 mg/kg; twice per day; 7 days) significantly suppresses proteinuria as well as reduces pseudocyst formation and podocyte loss in an AT1 receptor transgenic rat model of kidney disease[1].AC1903 (intraperitoneal injection; 50 mg/kg; twice per day; initiated on day 7 and treated for 1 week until day 14) initiatation on day 7 exhibits significant suppression of proteinuria with preserved podocyte numbers. Besides, AC1903 does not affect the mean arterial pressure (MAP) and exhibits no effect on body weight, blood urea nitrogen, or creatinine in Dahl S rats[1]. | Animal Model: | Hypertension-induced focal segmental glomerulosclerosis (FSGS) model in Dahl salt-sensitive rats[1] | | Dosage: | 50 mg/kg | | Administration: | Intraperitoneal injection; 50 mg/kg; twice per day; 7 days | | Result: | Inhibited the progression of proteinuric kidney disease by preserving podocytes. |
| Animal Model: | 6-week-old Dahl S rats received 2% NaCl for 1 week with severe, progressive proteinuric disease[1] | | Dosage: | 50 mg/kg | | Administration: | Intraperitoneal injection; 50 mg/kg; twice per day; initiated on day 7 and treated for 1 week until day 14 | | Result: | Decreased the rate of proteinuria when administered at the beginning of a high-salt diet and prevents progression when administered one week following initiation of a high-salt diet. |
| [storage]
Store at -20°C | [References]
1) Zhou?et al.?(2017),?A small-molecule inhibitor of TRPC5 ion channels suppresses progressive kidney disease in animal models; Science,?358?1332 |
|
|