¹²⁵I-SDF-1-CXCR4 ( IC50 = 13 nM ); HIV-1 (NL4.3 strain) ( IC50 = 1 nM ); HIV-1 (NL4.3 strain) ( IC50 = 9 nM ); HIV-1 (NL4.3 strain) ( IC50 = 3 nM ); HIV-1 (NL4.3 strain) ( IC50 = 26 nM )

Mavorixafor (AMD-070) 是一种有效的口服 CXCR4 拮抗剂，针对 CXCR4 125I-SDF 结合的 IC50 值为 13 nM，并且还抑制 MT-tropic HIV-1（NL4.3 株）的复制。 4 细胞和 PBMC 的 IC50 分别为 1 和 9 nM。 Mavorixafor (AMD-070) 对其他趋化因子受体（CCR1、CCR2b、CCR4、CCR5、CXCR1 和 CXCR2）没有影响[1]。 070) (6.6 µM) 显着抑制 B88-SDF-1 细胞的贴壁依赖性生长、迁移和基质胶侵袭[2]。

Mavorixafor (AMD-070) (2 mg/kg, po) 显着减少小鼠肺转移结节的数量，并降低小鼠体内人 Alu DNA 的表达，且体重不减轻[2]。

在 96 孔板上，以 5 × 10³ 细胞/孔接种含有 10% FCS 的 DMEM。 24 小时后，用或不用 2 µM AMD3100 或 6.6 µM AMD-070 处理细胞。采用 MTT 的测定用于量化 24 或 48 小时后的细胞数量[2]。

Absorption
In adults with WHIM syndrome, the mean (CV%) Cmax at steady-state is 3304 (58.6%) ng/mL and the AUC from 0 to 24 hours (AUC0-24h) is 13970 (58.4%) ngxh/mL following 400 mg once daily. Mavorixafor demonstrates nonlinear pharmacokinetics with greater than dose-proportional increases in Cmax and AUC0-24h over a dose range of 50 mg (0.125 times the recommended dosage) to 400 mg. Mavorixafor steady-state is reached after approximately 9 to 12 days at the highest approved recommended dosage in healthy subjects. Mavorixafor median (range) Tmax is 2.8 hours (1.9 to 4 hours) at the highest approved recommended dosage. Food decreases Cmax and AUC.

Route of Elimination
After a single oral dose of radiolabeled mavorixafor, 74.2% of the administered dose was recovered out of which 61.0% of administered radioactivity was recovered in feces and 13.2% (3% unchanged) was recovered in the urine over the 240-hour collection period in healthy subjects.

Volume of Distribution
Mavorixafor volume of distribution was 768 L in adults with WHIM syndrome.

Clearance
The mean (CV%) apparent clearance was 62 L/h (40%) following a single-dose administration of mavorixafor 400 mg in healthy subjects. Mavorixafor exhibits at least partial nonlinear apparent clearance; however, this is not clinically significant at the approved recommended dosage.

Protein Binding
In vitro, mavorixafor is >93% bound to human plasma proteins.

Metabolism / Metabolites
Mavorixafor is metabolized by CYP3A4 and, to a lesser extent, CYP2D6.

Biological Half-Life
The mean (CV%) terminal half-life was 82 h (34%) following a single-dose administration of mavorixafor 400 mg in healthy subjects.

Mavorixafor (AMD070) is an orally bioavailable small molecule; good oral bioavailability was observed in both rats and dogs [1]
- In CD-1 mice, after oral administration of Mavorixafor (AMD070) at 400 μg/animal, the drug was detected in the lung tissue, and its concentration varied over time, with the EC₉₀ (44 ng/mL) used as a reference threshold for pharmacodynamic activity [2]
- In C57BL/6 mice, following intraperitoneal administration of Mavorixafor (AMD070), the drug was distributed in plasma, liver, and lung tissues, with measurable concentrations at different time points [2]

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the use of mavorixafor during breastfeeding. The manufacturer recommends not breastfeeding treatment and for three weeks after the final dose.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

[1]. Discovery of novel small molecule orally bioavailable C-X-C chemokine receptor 4 antagonists that are potent inhibitors of T-tropic (X4) HIV-1 replication. J Med Chem. 2010 Apr 22;53(8):3376-88.

[2]. Effect of a novel orally bioavailable CXCR4 inhibitor, AMD070, on the metastasis of oral cancer cells. Oncol Rep. 2018 Jul;40(1):303-308.

Mavorixafor is a CXC chemokine receptor 4 (CXCR4) antagonist. It was first approved by the FDA on April 30, 2024, for the treatment of warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome, a genetic immunodeficiency disorder characterized by a reduced number of mature neutrophils and lymphocytes. WHIM syndrome is caused by mutations in the CXCR4 gene, which leads to overactivation of CXCR4 signalling pathways. Mavorixafor prevents the activation of CXCR4. As CXCR4 mutations have also been implicated in human immunodeficiency virus (HIV), Waldenstrom’s macroglobulinemia (WM), B-cell non-Hodgkin lymphoma, and solid tumours, including melanoma, mavorixafor is being investigated in these conditions.
Mavorixafor is a CXC Chemokine Receptor 4 Antagonist. The mechanism of action of mavorixafor is as a CXC Chemokine Receptor 4 Antagonist, and Cytochrome P450 2D6 Inhibitor, and Cytochrome P450 3A4 Inhibitor, and P-Glycoprotein Inhibitor.
Mavorixafor is an orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic and immune checkpoint inhibitory activities. Upon administration, mavorixafor selectively binds to CXCR4 and prevents the binding of CXCR4 to its ligand, stromal cell-derived factor 1 (SDF-1 or CXCL12). This inhibits receptor activation and results in decreased proliferation and migration of CXCR4-overexpressing tumor cells. In addition, inhibition of CXCR4 prevents the recruitment of regulatory T-cells and myeloid-derived suppressor cells (MDSCs) to the tumor microenvironment, thereby abrogating CXCR4-mediated immunosuppression and enabling the activation of a cytotoxic T-lymphocyte-mediated immune response against cancer cells. The G protein-coupled receptor CXCR4, which is upregulated in several tumor cell types, induces the recruitment of immunosuppressive cells in the tumor microenvironment, suppresses immune surveillance, and promotes tumor angiogenesis and tumor cell proliferation. It is also a co-receptor for HIV entry into T-cells.
MAVORIXAFOR is a small molecule drug with a maximum clinical trial phase of IV (across all indications) that was first approved in 2024 and is indicated for neoplasm and has 6 investigational indications.
a derivative of AMD3100; a CXCR4 blocker

C21H30CL3N5

458.855401515961

457.16

C, 54.97; H, 6.59; Cl, 23.18; N, 15.26

2309699-17-8

Mavorixafor; 558447-26-0; 880549-30-4

78357868

Light yellow to yellow solid powder

70.8

5

4

7

29

431

1

Cl.Cl.Cl.N(CC1=NC2C=CC=CC=2N1)(CCCCN)[C@@H]1C2C(=CC=CN=2)CCC1

FTHQTOSCZZCGHB-VLEZWVESSA-N

InChI=1S/C21H27N5.3ClH/c22-12-3-4-14-26(15-20-24-17-9-1-2-10-18(17)25-20)19-11-5-7-16-8-6-13-23-21(16)19;;;/h1-2,6,8-10,13,19H,3-5,7,11-12,14-15,22H2,(H,24,25);3*1H/t19-;;;/m0.../s1

N'-(1H-benzimidazol-2-ylmethyl)-N'-[(8S)-5,6,7,8-tetrahydroquinolin-8-yl]butane-1,4-diamine;trihydrochloride

Mavorixafor triHCl; Mavorixafor trihydrochloride; 2309699-17-8; Mavorixafor (trihydrochloride); AMD-070 trihydrochloride; C21H30Cl3N5; AMD-070 trihydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: ~150 mg/mL (~326.9 mM)
H2O: ~100 mg/mL (~217.9 mM)

配方 1 中的溶解度: ≥ 2.62 mg/mL (5.71 mM) (饱和度未知) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.62 mg/mL (5.71 mM) (饱和度未知) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 0.6 mg/mL (1.31 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 6.0 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 4 中的溶解度: ≥ 0.6 mg/mL (1.31 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，将100 μL 6.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 5 中的溶解度: ≥ 0.6 mg/mL (1.31 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 6.0 mg/mL 澄清 DMSO 储备液添加到 900 μL 玉米油中并混合均匀。

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配方 6 中的溶解度: 100 mg/mL (217.93 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。