货号:A195007
同义名:
AMD 3100; JM3100
Plerixafor是一种 CXCR4 受体拮抗剂,能够抑制 CXCL12 介导的趋化作用,IC50 分别为 44 nM 和 5.7 nM。


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| 产品名称 | CXCR1 ↓ ↑ | CXCR2 ↓ ↑ | CXCR4 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Reparixin | ✔ | 99%+ | |||||||||||||||||
| SB225002 |
+++
CXCR2, IC50: 22 nM |
99%+ | |||||||||||||||||
| Plerixafor |
++
CXCR4, IC50: 44 nM |
99% | |||||||||||||||||
| AMD 3465 6HBr | ✔ | 98% | |||||||||||||||||
| WZ811 |
++++
CXCR4, EC50: 0.3 nM |
99% | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 |
|
| 描述 | Through binding with CC- and CXC-chemokines, CCR and CXCR, the subsets of the chemokine receptor family can trigger an intracellular signal transduction cascade, thus mediating the recruitment of immune cells to the in£ammation or infection sites and implicated in several immuno-related disease states, organogenesis, angiogenesis and tumor growth and metastasis. AMD3100 is a selective antagonist of CXCR4 with IC50 values ranging in 0.01-0.13μg/ml for antagonizing SDF-1, but not itself, activated calcium flux in different cells tested, including CXCR4-transfected U87 and CD4 cells, freshly isolated PBMCs, SupT1, THP-1, HSB-2, Molt-4 and L1210 cells. The inhibitory effect of AMD3100 against the induced endocytosis of CXCR4 is selectively SDF-1-dependent but not phorbol ester. Pre-incubated with AMD3100 at concentration of 0.04, 0.2, 1, 5 and 25μg/ml could dose-dependently inhibit the SDF-1-induced (200 ng/ml) chemotaxis of human PBMCs[1]. In vivo study showed that intraperitoneal injection with 5mg/kg AMD3100 can alter the potential of mesenchymal stem cells mobilization induced by different growth factors, including IGF-1, SCF, PDGF and VEGF, in mice, which may be mediated through Akt/PI3K, MEK1/2-Erk1/2 and smad2/3 as key signaling pathways[2]. |
| 作用机制 | Not found |
| Concentration | Treated Time | Description | References | |
| KU812F cells | 50 μM | 3 h | Reduced adhesion of CML cells to BM microenvironment components | Leukemia. 2012 May;26(5):985-90. |
| KU812F cells | 50 μM | 3 h | Reduced drug resistance of CML cells to nilotinib | Leukemia. 2012 May;26(5):985-90. |
| EJ cells | 50 μM | 24 h | Inhibited the proliferation and migration capacity of EJ cells by blocking CXCR4 downstream signaling | Sci Adv. 2023 Mar;9(9):eabq8225. |
| MDA-MB-231 cells | 10 μg/mL | 1 h | To study the uptake of Plerixafor-modified nanocarriers in CXCR4-expressing MDA-MB-231 cells, results showed that Plerixafor-modified nanocarriers had a higher uptake rate in CXCR4-expressing cells compared to unmodified carriers. | Biomacromolecules. 2015 Aug 10;16(8):2412-7. |
| Administration | Dosage | Frequency | Description | References | ||
| Mice | Radiation-induced wound healing deficit model | Subcutaneous injection | 5 mg/kg | Single injection | Plerixafor combined with G-CSF enhanced the efficacy of MSC-FMB in correcting radiation-induced wound healing deficits | J Invest Dermatol. 2013 Feb;133(2):553-61 |
| Mice | Spinal cord injury model | Subcutaneous injection | 5 mg/kg | Once daily for 3 days | Plerixafor treatment increased the number of HSPCs released into the blood by more than 6-fold, with a corresponding increase in the number of HSPCs found in the spleen, and reversed the post-SCI leukopenia. | Nat Commun. 2020 Jul 24;11(1):3702 |
| Mice | BCR-ABL-positive leukemia mouse model | Subcutaneous injection | 5 mg/kg | Once daily for 10 days | Reduced leukemia burden and prolonged survival | Leukemia. 2012 May;26(5):985-90. |
| Nude mice | EJ xenograft model | Intravenous injection | 100 μM, 100 μl | Once every 2 days for a total of five times | Plerixafor significantly inhibited tumor growth, with a mean tumor volume of 647±147 mm3, compared to 1086±257 mm3 in the saline group | Sci Adv. 2023 Mar;9(9):eabq8225. |
| Rhesus macaque | Rhesus gene therapy model | Intravenous injection | 1 mg/kg | Single dose, after 5 days of G-CSF administration | Mobilization of CD34+ cells for gene therapy model | Nat Commun. 2023 Oct 12;14(1):6291 |
| Dose | Mice[3]: 0.625 mg/kg - 10 mg/kg (s.c.) Rat[3]: 25 mg/kg (s.c.), 2 mg/kg (i.v.) | ||||||||||||||||||
| Administration | s.c., i.v. | ||||||||||||||||||
| Pharmacokinetics |
|
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
| NCT01164475 | - | Completed | - | - | |
| NCT01711073 | End Stage Liver DIsease | Phase 1 | Unknown | September 2013 | United States, New Jersey ... 展开 >> University of Medicine and Dentistry of New Jersey Recruiting Newark, New Jersey, United States, 07101 Contact: Baburao Koneru, MD koneruba@umdnj.edu 收起 << |
| NCT01123499 | - | Recruiting | - | United States, Maryland ... 展开 >> National Institutes of Health Clinical Center, 9000 Rockville Pike Recruiting Bethesda, Maryland, United States, 20892 Contact: Sandra Maxwell, B.S.N. 301-402-1773 maxwells@niaid.nih.gov 收起 << | |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
1.99mL 0.40mL 0.20mL |
9.94mL 1.99mL 0.99mL |
19.89mL 3.98mL 1.99mL |
|
| CAS号 | 110078-46-1 |
| 分子式 | C28H54N8 |
| 分子量 | 502.78 |
| SMILES Code | N1(CC2=CC=C(CN3CCNCCCNCCNCCC3)C=C2)CCNCCCNCCNCCC1 |
| MDL No. | MFCD05662218 |
| 别名 | AMD 3100; JM3100; JKL 169; Mozobil; SDZ SID 791; SID791 |
| 运输 | 蓝冰 |
| InChI Key | YIQPUIGJQJDJOS-UHFFFAOYSA-N |
| Pubchem ID | 65015 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Keep in dark place, inert atmosphere, 2-8°C |
| 溶解方案 |
DMSO: 1.5 mg/mL(2.98 mM),配合低频超声,水浴加热至45℃,并调节pH至5,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 无水乙醇: 45 mg/mL(89.5 mM),配合低频超声助溶,注意:无水乙醇开封后,易挥发,也会吸收空气中的水分,导致溶解能力下降,请避免使用开封较久的乙醇 以下溶解方案都请先按照体外实验的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
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