| Identification | Back Directory | [Name]
Hydrocinnamate | [CAS]
514814-49-4 | [Synonyms]
PMX-205
Hydrocinnamate
deamino-Phe-Orn(1)-Pro-D-Cha-Trp-Arg-(1)
L-Arginine, N2-(1-oxo-3-phenylpropyl)-L-ornithyl-L-prolyl-3-cyclohexyl-D-alanyl-L-tryptophyl-, (5→1)-lactam | [Molecular Formula]
C45H62N10O6 | [MDL Number]
MFCD31657373 | [MOL File]
514814-49-4.mol | [Molecular Weight]
839.04 |
| Chemical Properties | Back Directory | [density ]
1.38±0.1 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [pka]
13.40±0.70(Predicted) | [Water Solubility ]
Soluble in 20% ethanol / sterile Water |
| Hazard Information | Back Directory | [Uses]
PMX 205 is a potent complement C5a receptor (C5aR; CD88) antagonist. | [Definition]
ChEBI: PMX-205 is a homodetic cyclic peptide resulting from the formal condensation of the carboxy group of N(2)-(3-phenylpropanoyl)-L-ornithyl-L-prolyl-3-cyclohexyl-D-alanyl-L-tryptophyl-L-arginine with the 5-amino group of the N(2)-acylornithyl residue. It has a role as an antagonist, an anti-inflammatory agent and a C5a receptor antagonist. It is an azamacrocycle and a homodetic cyclic peptide. | [in vivo]
PMX 205 (PMX205) is an orally active, selective C5aR antagonist. Animals treated with PMX 205 (1 mg/kg/day, oral) displays a significant extension of survival time and a reduction in end-stage motor scores, as compared with vehicle-treated rats. PMX 205-treated animals also display reduced levels of astroglial proliferation in the lumbar spinal cord. SOD1G93A rats are orally dosed with PMX 205 (1 mg/kg/day) from two time points (days 28 and 70) before the onset of major clinical symptoms. Both treatment groups have a significant extension in survival time compared with untreated rats (p=0.022, day 28; p=0.015, day 70), with no clear differences in outcomes between the two treatment regimens[2]. Tg2576 mice are treated with PMX 205 (PMX205) at 20 μg/mL in the drinking water (n=17) from 12 to 15 mo of age, the time frame at which there is a rapid accumulation of amyloid deposits in these animals. Untreated Tg2576 animals (n=11) are used as controls. After 3 mo, animals treated with PMX 205 show significantly less fibrillar plaque load (thioflavine reactivity) than do untreated animals. In 3×Tg mice, PMX 205 also significantly reduces hyperphosphorylated tau (69%)[3]. | [storage]
Store at -20°C | [References]
[1] Kosni NN, et al. Expression of complement C5a receptor and the viability of 4T1 tumor cells following agonist-antagonist treatment. J Cancer Res Ther. 2016 Apr-Jun;12(2):590-6. DOI:10.4103/0973-1482.146066
[2] Woodruff TM, et al. The complement factor C5a contributes to pathology in a rat model of amyotrophic lateral sclerosis. J Immunol. 2008 Dec 15;181(12):8727-34. DOI:10.4049/jimmunol.181.12.8727
[3] Fonseca MI, et al. Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease. J Immunol. 2009 Jul 15;183(2):1375-83. DOI:10.4049/jimmunol.0901005 |
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BOC Sciences
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https://www.bocsci.com |
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