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Fig. 1 · Structure
Cat. No.
A11315
CAS No.
558447-26-0
Formula
C21H27N5
Mol. Weight
349.5

Documents & Downloads

Mavorixafor (AMD 070)

Cat. No. A11315 CAS 558447-26-0

CXCR4 antagonist

AMD 070 is a CXCR4 chemokine receptor antagonist.

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Publications for Mavorixafor

2 publications citing this product

  1. Uchida D, .et al. , Oncol Rep, 2018, Jul;40(1):303-308 PMID: 29749473
  2. Mamoru Morimoto, .et al. , BMC Cancer, 2016, 16: 305 PMID: 27175473
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Biological Activity

Bioactivity / Mechanism

Mavorixafor (AMD070) occupies the CXCR4 orthosteric pocket. A cryo-EM study using AMD070 trihydrochloride and an engineered human receptor resolved contacts involving Asp97 and Glu288 across the binding pocket. This supports a structural explanation of CXCR4 antagonism; it does not establish potency for the catalog free-base material. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
125I-SDF-CXCR4 IC50 13 nM
HIV-1 (NL4.3 strain) 1 nM (IC50, in MT-4 cells)
HIV-1 (NL4.3 strain) 9 nM (IC50, in PBMCs)
HIV-1 (NL4.3 strain) 3 nM (IC90, in MT-4 cells)
HIV-1 (NL4.3 strain) 26 nM (IC90, in PBMCs)

In Vitro Studies

At 6.6 µM, AMD070 reduced wound closure over 48 h in B88-SDF-1 oral cancer cells relative to untreated cells. This single-concentration motility experiment used an engineered SDF-1-expressing model. [2]

AMD070 binding in an engineered CXCR4 cryo-EM complex

Biochemical assay · Human CXCR4κOR–Nb6 complex; receptor contains L125W/T240P and a substituted ICL3 [1]

AMD070 was resolved in the orthosteric pocket, involving major and minor subpockets. The modeled contacts include Asp97 and Glu288. This is a structural observation in an engineered receptor.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Global resolution of AMD070–CXCR4κOR–Nb6 reconstructionresolution 3.2 Å[1]

Literature-Reported Treatment Conditions

Method
Cryo-EM of purified antagonist-bound receptor complex
Reported limits
No assay IC50 or cellular treatment dose adopted; SI validation plots not retrieved.
Methods and source locations

Compound reported in the paper: Mavorixafor (AMD070); Compound label in the paper: AMD070

Qualitative binding mechanism of the AMD070 moiety; no salt equivalence, dose conversion or lot validation.

Results: Cryo-EM Structures; binding pattern; Figs. 1C–D and 3A–C; Materials and Methods: CXCR4 Antagonists and Construct Design

Global resolution of AMD070–CXCR4κOR–Nb6 reconstruction: Single-particle cryo-EM — Results: Cryo-EM Structures; Fig. 1C–D

Reduced wound closure in B88-SDF-1 oral cancer cells

Cell-based study · B88-SDF-1 oral cancer transfectants; B88-mock comparator [2]

AMD070 reduced the enhanced wound closure of B88-SDF-1 cells relative to untreated cells. AMD3100 was a separate comparator, not a combination.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Wound closure area at 48 hReduced versus untreated B88-SDF-1; P<0.05[2]

Literature-Reported Treatment Conditions

Treatment concentration
6.6 µM
Exposure duration
48 h
Method
Wound-healing assay
Co-treatment
None; AMD3100 at 2 µM tested separately
Reported limits
Drug vehicle not specified in the wound-healing method; no exact closure magnitude extracted.
Methods and source locations

Compound reported in the paper: Mavorixafor (AMD070); Compound label in the paper: AMD070

Single-concentration cell motility result; does not establish generalized cytotoxicity, invasion potency or clinical efficacy.

Materials and methods: Wound healing assay; Fig. 3A–B

Wound closure area at 48 h: Wound-healing assay; triplicate; error bars SD; one-way ANOVA — Fig. 3A–B and caption; Wound healing assay

In Vivo Studies

Daily oral AMD070 at 2 mg/kg reduced experimental lung colonization by B88-SDF-1 cells in nude mice. Histology detected lung metastases in 2/10 treated mice and 5/9 saline controls at day 49. [2]

In bleomycin-injured mice, oral AMD070 improved survival but did not reduce endpoint lung fibrosis or inflammation among survivors. In a separate CCl4 liver-injury experiment, intraperitoneal AMD070 did not reduce hepatic fibrosis. These results limit a general antifibrotic interpretation. [3]

Experimental lung metastasis in nude mice

Animal study · Eight-week-old BALB/c nude mice bearing intravenously introduced B88-SDF-1 cells [2]

The AMD070 group had fewer mice with lung metastases and fewer tumor nests than saline controls at day 49.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Mice with histologically detected lung metastasesincidence Saline: 5/9; AMD070: 2/10[2]
Reported lung tumor nest countsnest count Saline: 16; AMD070: 3; P<0.05[2]

Conditions shared by the study groups

Route
Oral
Frequency
Daily
Treatment course
49-day observation; exact initial dose day unspecified
Vehicle
0.2 mL; saline comparator
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AMD070 versus saline
2 mg/kg		Equal volume of salineLung metastases: 2/10 versus 5/9 mice; nest counts 3 versus 16.[2]
AMD070 versus saline
Model: BALB/c nude mice; B88-SDF-1 lung colonization
Reported limits: Dose retained as reported; no inference of per-mouse mean from nest totals. Sex not specified.
Methods and source locations

Compound reported in the paper: Mavorixafor (AMD070); Compound label in the paper: AMD070

Experimental lung colonization model; no spontaneous metastasis or human efficacy inference.

Mice and the in vivo study; Results: lung metastasis; Fig. 4A

Mice with histologically detected lung metastases: Lung H&E histology — Results: lung metastasis; Fig. 4A

Reported lung tumor nest counts: Histology; source reports one-way ANOVA — Fig. 4A and caption

AMD070 versus saline · Mice and the in vivo study; Fig. 4A

Survival benefit without reduced pulmonary fibrosis

Animal study · Female six-week-old CD-1 mice with bleomycin-induced lung injury; initially n=10/group [3]

AMD070 improved endpoint survival, while surviving treated mice had no reduction in lung inflammation or fibrosis. Histology comparisons are conditional on survival and include unequal final group sizes.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Survival through day 22survival BLM plus AMD070: 90%; BLM plus acetate buffer: 40%[3]
Fibrotic surface area in surviving micepercent fibrosis BLM plus vehicle: 3.7% (SEM ±1.1); BLM plus AMD070: 10.5% (SEM ±2.5)[3]
Inflammatory surface area in surviving micepercent inflammation BLM plus vehicle: 5.4% (SEM ±2.4); BLM plus AMD070: 14.2% (SEM ±3.0)[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Treatment course
Day 1 through day 21; endpoint day 22
Vehicle
30 mM acetate buffer, pH 5
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AMD070 in bleomycin lung injury
400 µg/mouse in 200 µL		BLM plus acetate buffer; uninjured PBS plus acetate buffer also includedSurvival 90% versus 40%; final histology n=9 versus n=4. No reduction in fibrosis or inflammation.[3]
AMD070 in bleomycin lung injury
Model: Female CD-1 mice; initially n=10/group
Reported limits: Final n labels in Fig. 6 refer to survivors, not initial group size.
Methods and source locations

Compound reported in the paper: Mavorixafor (AMD070); Compound label in the paper: AMD070

Model-specific survival and histology; no general antifibrotic efficacy or free-base lot validation.

Murine model of pulmonary fibrosis; Histology methods; Results and Figs. 4–6

Survival through day 22: Kaplan–Meier observation; humane-endpoint euthanasia counted in mortality — Results: pulmonary efficacy; Fig. 6

Fibrotic surface area in surviving mice: Masson’s Trichrome; blinded image analysis; final n=4 and n=9, respectively — Results: pulmonary efficacy; Fig. 5A

Inflammatory surface area in surviving mice: H&E histology; blinded image analysis; final n=4 and n=9, respectively — Results: pulmonary efficacy; Fig. 4A

AMD070 in bleomycin lung injury · Pulmonary model methods; Figs. 4–6

No reduction of hepatic fibrosis in the CCl4 model

Animal study · Female eleven-week-old C57BL/6 mice with carbon-tetrachloride-induced hepatic fibrosis [3]

AMD070 did not reduce the fibrotic liver area compared with injured PBS controls. Final group sizes were 9, 6 and 7 for oil control, CCl4 control and CCl4 plus AMD070.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Mean Picrosirius Red-positive liver areapercent fibrosis Oil plus PBS: 0.53%; CCl4 plus PBS: 3.2%; CCl4 plus AMD070: 3.6%[3]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
5 days/week; withheld on the two CCl4 dosing days
Treatment course
4 weeks; beginning one day before first CCl4; endpoint one day after last AMD070
Vehicle
PBS
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AMD070 in CCl4 hepatic fibrosis
50 mg/kg		CCl4 plus PBS; oil plus PBS baseline controlFibrotic liver area 3.6% versus 3.2%; no treatment-associated reduction reported.[3]
AMD070 in CCl4 hepatic fibrosis
Model: Female C57BL/6 mice
Reported limits: Reported final analyzed group sizes, not initial randomized sample sizes.
Methods and source locations

Compound reported in the paper: Mavorixafor (AMD070); Compound label in the paper: AMD070

Negative finding confined to this regimen and model.

Murine model of hepatic fibrosis; Histology methods; Fig. 9 and associated Results

Mean Picrosirius Red-positive liver area: Blinded histological area scoring; three liver sections per animal — Results: hepatic efficacy; Fig. 9A

AMD070 in CCl4 hepatic fibrosis · Hepatic model methods; Fig. 9 and Results

Specifications

Manufacturer Adooq Bioscience
Actions Antagonist
CAS Number 558447-26-0
Applications CXCR4 antagonist
Formula C21H27N5
Molecular Weight 349.5
Synonyms AMD070
SMILES
C1C[C@@H](C2=C(C1)C=CC=N2)N(CCCCN)CC3=NC4=CC=CC=C4N3

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Sang X, Jiao H, Meng Q, et al. Structural mechanisms underlying the modulation of CXCR4 by diverse small-molecule antagonists Proceedings of the National Academy of Sciences of the United States of America (2025). PMID: 40063796 DOI: 10.1073/pnas.2425795122 Source material
  2. [2] Uchida D, Kuribayashi N, Kinouchi M, et al. Effect of a novel orally bioavailable CXCR4 inhibitor, AMD070, on the metastasis of oral cancer cells Oncology reports (2018). PMID: 29749473 DOI: 10.3892/or.2018.6400 Source material
  3. [3] Chow LN, Schreiner P, Ng BY, et al. Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmonary Fibrosis and Carbon Tetrachloride (CCl4) Induced Hepatic Fibrosis in Mice PloS one (2016). PMID: 26998906 DOI: 10.1371/journal.pone.0151765 Source material

Publications

2 publications citing this product

  1. Uchida D, .et al. , Oncol Rep, 2018, Jul;40(1):303-308 PMID: 29749473
  2. Mamoru Morimoto, .et al. , BMC Cancer, 2016, 16: 305 PMID: 27175473

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