PMX-53 (3D53) is a synthetic peptidic and a potent and orally active complement C5a receptor (CD88) antagonist with an IC₅₀ of 20 nM. PMX-53 is also a low-affinity MrgX2 agonist that stimulates MrgX2-mediated mast cell degranulation. PMX-53 specifically binds to C5aR1 and does not bind to the second C5aR (C5L2) and C3aR. PMX-53 has anti-inflammatory, anticancer and antiatherosclerotic effects^{[1][2][3][4][5][6]}.

IC50: 20 nM (Complement C5a receptor)^[4]
MrgX2^[1]

PMX-53 is a potent CD88 antagonist and inhibits C5a-induced neutrophil myeloperoxidase release and chemotaxis with IC₅₀ values of 22 nM and 75 nM, respectively^[1].
PMX-53 (10 nM) inhibits C5a-induced Ca²⁺ mobilization in HMC-1 cells, but at higher concentrations( ≥30 nM) it causes degranulation in LAD2 mast cells, CD34⁺ cell-derived mast cells, and RBL-2H3 cells stably expressing MrgX2. Replacement of Trp with Ala and Arg with dArg abolishes the ability of PMX-53 to inhibit C5a-induced Ca²⁺ mobilization in HMC-1 cells and to cause degranulation in RBL-2H3 cells expressing MrgX2^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

PMX-53 (0.3-3 mg/kg; subcutaneous injection; once; male Wistar rats) treatment inhibits the hypernociception induced by zymosan-activated serum and C5a but not by the direct-acting hypernociceptive mediators, prostaglandin E2 and dopamine^[2].
Local pretreatment of rats with PMX-53 (60-180 μg per paw) inhibits zymosan-, carrageenan-, lipopolysaccharide (LPS)- and antigen-induced hypernociception^[2].
Pharmacokinetic analyses have shown that PMX-53 (3D53) appears in the plasma within 5 min of oral administration (3 mg/kg) to rats, with peak blood levels of approximately 0.3 µM beingreached within 20 min The plasma elimination half-life wasapproximately 70 min in this case^[3].
The non-acetylated version of PMX-53 (3D53) binds to isolated mouse neutrophils with a K_d value of 30 nM (mouse C5a binds with a K_d value of 0.3 nM) and inhibits mouse C5a-induced chemotaxis with an IC₅₀ value of 0.5 nM^[3].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

896.09

C₄₇H₆₅N₁₁O₇

219639-75-5

F-{Orn}-P-{d-Cha}-WR (Lactam bridge: Orn2- Arg6)

Room temperature in continental US; may vary elsewhere.

Protect from light, stored under nitrogen

Powder	-80°C	2 years
	-20°C	1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

In Vitro: 

DMSO : 125 mg/mL (139.49 mM; Need ultrasonic)

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.08 mg/mL (2.32 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (2.32 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.08 mg/mL (2.32 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (2.32 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.08 mg/mL (2.32 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (2.32 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Subramanian H, et al. PMX-53 as a dual CD88 antagonist and an agonist for Mas-related gene 2 (MrgX2) in human mast cells. Mol Pharmacol. 2011 Jun;79(6):1005-13.

  [2]. Ting E, et al. Role of complement C5a in mechanical inflammatory hypernociception: potential use of C5a receptor antagonists to control inflammatory pain. Br J Pharmacol. 2008 Mar;153(5):1043-53.

  [3]. Holland MC, et al. Synthetic small-molecule complement inhibitors. Curr Opin Investig Drugs. 2004 Nov;5(11):1164-73.

  [4]. Finch AM, et al. Low-molecular-weight peptidic and cyclic antagonists of the receptor for the complement factor C5a. J Med Chem. 1999 Jun 3;42(11):1965-74.

  [5]. Manthey HD, et al. Complement C5a inhibition reduces atherosclerosis in ApoE-/- mice. FASEB J. 2011 Jul;25(7):2447-55.

  [6]. Vadrevu SK, et al. Complement c5a receptor facilitates cancer metastasis by altering T-cell responses in the metastatic niche. Cancer Res. 2014 Jul 1;74(13):3454-65.