| Identification | Back Directory | [Name]
(2(S)-[1-(3,5-Dichlorophenylsulfonyl)-L-prolylaMino]-4-[N-Methyl-N-[2-[4-[3-(2-Methylphenyl)ureido]phenyl]acetyl]-L-leucylaMino]butyric acid ) | [CAS]
327613-57-0 | [Synonyms]
BIO 5192
AMD 15057
BIO-5192
(BIO5192)
(2(S)-[1-(3,5-Dichlorophenylsulfonyl)-L-prolylaMino]-4-[N-Methyl-N-[2-[4-[3-(2-Methylphenyl)ureido]phenyl]acetyl]-L-leucylaMino]butyric acid )
(S)-2-((S)-1-((3,5-dichlorophenyl)sulfonyl)pyrrolidine-2-carboxamido)-4-((S)-4-methyl-2-(N-methyl-2-(4-(3-(o-tolyl)ureido)phenyl)acetamido)pentanamido)butanoic acid
(2S)-2-[[[(2S)-1-[(3,5-Dichlorophenyl)sulfonyl]-2-pyrrolidinyl]carbonyl]amino]-4-[[(2S)-4-methyl-2-[methyl[2-[4-[[[(2-methylphenyl)amino]carbonyl]amino]phenyl]acetyl]amino]-1-oxopentyl]amino]butanoic acid
Butanoic acid, 2-[[[(2S)-1-[(3,5-dichlorophenyl)sulfonyl]-2-pyrrolidinyl]carbonyl]amino]-4-[[(2S)-4-methyl-2-[methyl[2-[4-[[[(2-methylphenyl)amino]carbonyl]amino]phenyl]acetyl]amino]-1-oxopentyl]amino]-, (2S)- | [Molecular Formula]
C38H46Cl2N6O8S | [MOL File]
327613-57-0.mol | [Molecular Weight]
817.78 |
| Chemical Properties | Back Directory | [Melting point ]
134 - 136°C | [density ]
1.380±0.06 g/cm3(Predicted) | [storage temp. ]
Hygroscopic, -20°C Freezer, Under inert atmosphere | [solubility ]
DMSO (Slightly) | [form ]
Solid | [pka]
3.52±0.10(Predicted) | [color ]
White to Off-White |
| Hazard Information | Back Directory | [Uses]
BIO 5192, is selective, potent inhibitor of integrin α4β1 with an IC50 value of 1.8 ± 0.7 nM. α4β1 regulates the migration of lymphocytes into inflamed tissues, and thus BIO 5192 cna act as an antiinflammatory agent. | [Biological Activity]
bio5192 is a small molecule inhibitor of integrin α4β1 with an ic50 value of 1.8 ± 0.7 nm [1].integrin α4β1 is important in inflammatory processes. in the inflammatory processes, α4β1 regulates the migration of lymphocytes into inflamed tissues [1].in assays using cells expressing α4β7, α9β1, α2β1, and αiibβ3, bio5192 showed high selectivity for α4β1. the affinity of bio5192 for α4β1 was 250- to 1000-fold higher than for α4β7 that shared many ligands the same as α4β1. bio5192 bound even less tightly to α2β1 and αiibβ3. a significant but low level (kd=140 nm) of binding was seen on α9β1 in buffer containing 1 mm mn2+ [1].after 24 h of bio5192 treatment, the lymphocyte count rose about 1.5-fold. half as many cells as when ta-2 was given were released into the circulation following the treatment with bio5192. data showed that bio5192 remained bound to 100% of the α4β1 receptors for 24 h and 50% for 48 h. rats treated with bio5192 at 30 mg/kg, s.c. showed a 1- to 2-day shift when dosed q.d. and a 3-day delay in the onset of disease eae when dosed b.i.d. compared with the control groups. the delay in the onset of eae in the bio5192-treated group was consistent with the finding that bound bio5192 would occupy α4β1 long beyond the point at which the bio5192 was no longer detected in blood [1]. | [in vivo]
The combination of BIO5192 (1 mg/kg; i.v.) and Plerixafor (5 mg/kg; s.c.) exert an additive effect on progenitor mobilization[1].
BIO5192 (30 mg/kg; s.c; bid; during days 5 through 14) delays paralysis associated with EAE (experimental autoimmune encephalomyelitis)[2].
BIO5192 (1 mg/kg, i.v.) shows the terminal half-life is 1.1 hours. BIO5192 (3, 10, and 30 mg/kg; s.c.) shows half-lives of 1.7, 2.7, and 4.7 hours, respectively. The blood plasma curves show that the AUC for the s.c. route of administration increased about 2.5-fold from 5,460 h*ng/ml for the 3 mg/kg dose to 14,175 h*ng/ml for the 30 mg/kg[1]. | Animal Model: | C57BL/6J x 129Sv/J F1 mice[1] | | Dosage: | 1 mg/kg (with Plerixafor: 5 mg/kg) | | Administration: | I.v. | | Result: | Exerted an additive effect on progenitor mobilization.
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| Animal Model: | Healthy female Lewis rats weighing 150g[2] | | Dosage: | 30 mg/kg | | Administration: | S.c; bid; during days 5 through 14 | | Result: | Showed a 3-day delay in onset of disease.
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| [IC 50]
α4β1: 1.8 nM (IC50); α9β1: 138 nM (IC50); α2β1: 1053 nM (IC50); α4β7: >500 nM (IC50) | [storage]
Store at -20°C | [References]
[1]. leone dr, giza k, gill a, et al. an assessment of the mechanistic differences between two integrin α4β1 inhibitors, the monoclonal antibody ta-2 and the small molecule bio5192, in rat experimental autoimmune encephalomyelitis[j]. journal of pharmacology and experimental therapeutics, 2003, 305(3): 1150-1162. |
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| Company Name: |
BOC Sciences
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| Tel: |
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| Website: |
https://www.bocsci.com |
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