Biological ActivityPMX 53 is a potent C5a receptor antagonist (IC50 = 20 nM). Also MrgX2 agonist. Stimulates MrgX2-mediated mast cell degranulation. Also inhibits C5a-induced hypernociception in rats, inhibits lung metastasis in a mouse breast cancer model and reduces atherosclerotic lesions in a mouse model of atherosclerosis.
Negative Control also available.
(Modifications: Phe-1 = N-terminal Ac, X-2 = Orn, X-4 = D-Cha, Lactam bridge: Orn-2 to Arg-6 )
The technical data provided above is for guidance only.
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Tocris products are intended for laboratory research use only, unless stated otherwise.
PMX-53 as a dual CD88 antagonist and an agonist for Mas-related gene 2 (MrgX2) in human mast cells.
Subramanian et al.
Complement C5a inhibition reduces atherosclerosis in ApoE-/- mice.
Manthey et al.
FASEB J, 2011;25:2447
Development and validation of a LC-MS/MS assay for pharmacokinetic studies of complement C5a receptor antagonists PMX53 and PMX205 in mice.
Kumar et al.
Role of complement C5a in mechanical inflammatory hypernociception: potential use of C5a receptor antagonists to control inflammatory pain.
Ting et al.
Low-molecular-weight peptidic and cyclic antagonists of the receptor for the complement factor C5a.
Finch et al.
Complement c5a receptor facilitates cancer metastasis by altering T-cell responses in the metastatic niche.
Vadrevu et al.
Cancer Res., 2014;74:3454
Citation for PMX 53
The citations listed below are publications that use Tocris products. Selected citations for PMX 53 include:
1 Citation: Showing 1 - 1
Orthosteric and allosteric action of the C5a receptor antagonists.
Nat Struct Mol Biol 2018;25:472
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We used this inhibitor to study the biological activity of staphylococcal leukocidin PVL, which uses C5aR as a receptor to target host immune cells. We treated neutrophils with different concentrations (2.5, 5, and 10 uM) of pmx-53 for 1 h before incubated with 1 ug/ml PVL, and the cytotoxicity of treated cells was measured by LDH assay kit. As expected, pmx-53 treatment resulted in a dose-dependent reduction of PVL cytotoxicity to neutrophils.