AMD 3465CXCR4 antagonist,potent and selective CAS# 185991-24-6 |
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Quality Control & MSDS
3D structure
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| Cas No. | 185991-24-6 | SDF | Download SDF |
| PubChem ID | 483559 | Appearance | Powder |
| Formula | C24H38N6 | M.Wt | 410.6 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | AMD3465,AMD-3465 | ||
| Solubility | Soluble in DMSO | ||
| Chemical Name | N-(pyridin-2-ylmethyl)-1-[4-(1,4,8,11-tetrazacyclotetradec-1-ylmethyl)phenyl]methanamine | ||
| SMILES | C1CNCCNCCCN(CCNC1)CC2=CC=C(C=C2)CNCC3=CC=CC=N3 | ||
| Standard InChIKey | CWJJHESJXJQCJA-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C24H38N6/c1-2-13-29-24(5-1)20-28-19-22-6-8-23(9-7-22)21-30-17-4-12-26-15-14-25-10-3-11-27-16-18-30/h1-2,5-9,13,25-28H,3-4,10-12,14-21H2 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | AMD 3465 is a potent, selective CXCR4 antagonist, and inhibits SDF-1α-ligand binding with Ki of 41.7 nM.In Vitro:The affinity of AMD3465 is 8-fold higher compared with AMD3100, in competition against the radiolabeled monoclonal antibody raised against CXCR4, 12G5. The affinity of AMD3465 is decreased >5000-fold in (D262N)-CXCR4 and 1913-fold in (A175F)-CXCR4. AMD3465 appears to interact with HisVII:-02 at the extracellular end of TM-VII (at the interface to extracellular loop 3) and HisIII:05. Both of these His residues are facing right into the main binding pocket of CXCR4[1]. AMD3465 inhibits 125I-SDF-1α ligand binding to CCRF-CEM cells. AMD3465 inhibits CXCR4 activation as measured by GTP binding with an IC50 of 10.38±1.99 nM, and inhibits SDF-1α mediated calcium flux with an IC50 of 12.07±2.42 nM[2].In Vivo:AMD3465 (5 mg/kg, s.c.) significantly elevates total white blood cells in DBA/2, C57Bl/6 and BALB/c mice between 0.5 and 2 h. AMD3465 significantly increases the specific cell populations in all three strains of mice included neutrophils, lymphocytes, and monocytes[2]. References: | |||||
AMD 3465 Dilution Calculator
AMD 3465 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4355 mL | 12.1773 mL | 24.3546 mL | 48.7092 mL | 60.8865 mL |
| 5 mM | 0.4871 mL | 2.4355 mL | 4.8709 mL | 9.7418 mL | 12.1773 mL |
| 10 mM | 0.2435 mL | 1.2177 mL | 2.4355 mL | 4.8709 mL | 6.0887 mL |
| 50 mM | 0.0487 mL | 0.2435 mL | 0.4871 mL | 0.9742 mL | 1.2177 mL |
| 100 mM | 0.0244 mL | 0.1218 mL | 0.2435 mL | 0.4871 mL | 0.6089 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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IC50: 10.38 ± 1.99 nM for CXCR4 activation as measured by GTP binding
CXCR4 is widely expressed in multiple cell types, and involved in neonatal development, hematopoiesis, and lymphocyte trafficking and homing. Additionally CXCR4 is a co-receptor for HIV. Small molecule antagonists of CXCR4 thus have therapeutic potential. AMD3465 is an N-pyridinylmethylene monocyclam CXCR4 antagonist blocking infection of T-tropic, CXCR4-using HIV.
In vitro: Using the CCRF-CEM T-cell line expressing CXCR4 previous authors have demonstrated that AMD3465 is an antagonist of SDF-1 ligand binding, and inhibits SDF-1 mediated signaling as shown by inhibition of GTP binding, calcium flux, and inhibition of chemotaxis. AMD3465 does not inhibit chemokine-stimulated calcium flux in cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7, nor does it inhibit binding of LTB4 to its receptor, BLT1 [1].
In vivo: AMD3465 caused leukocytosis when subcutaneously administered in mice and dogs, with peak mobilization occurring between 0.5 and 1.5 h following subcutaneous dosing in mice and with maximum peak plasma concentration of compound preceding peak mobilization in dogs, demonstrating that AMD3465 has the potential to mobilize hematopoietic stem cells. These data demonstrate the therapeutic potential for the CXCR4 antagonist AMD3465 [1].
Clinical trials: Currenlty no clinical data are available.
Reference:
[1] Bodart V, Anastassov V, Darkes MC, Idzan SR, Labrecque J, Lau G, Mosi RM, Neff KS, Nelson KL, Ruzek MC, Patel K, Santucci Z, Scarborough R, Wong RS, Bridger GJ, Macfarland RT, Fricker SP. Pharmacology of AMD3465: a small molecule antagonist of the chemokine receptor CXCR4. Biochem Pharmacol. 2009;78(8):993-1000.
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Blocking CXCR4-mediated cyclic AMP suppression inhibits brain tumor growth in vivo.[Pubmed:17234775]
Cancer Res. 2007 Jan 15;67(2):651-8.
The chemokine CXCL12 and its cognate receptor CXCR4 regulate malignant brain tumor growth and are potential chemotherapeutic targets. However, the molecular basis for CXCL12-induced tumor growth remains unclear, and the optimal approach to inhibiting CXCR4 function in cancer is unknown. To develop such a therapeutic approach, we investigated the signaling pathways critical for CXCL12 function in normal and malignant cells. We discovered that CXCL12-dependent tumor growth is dependent upon sustained inhibition of cyclic AMP (cAMP) production, and that the antitumor activity of the specific CXCR4 antagonist AMD 3465 is associated with blocking cAMP suppression. Consistent with these findings, we show that pharmacologic elevation of cAMP with the phosphodiesterase inhibitor Rolipram suppresses tumor cell growth in vitro and, upon oral administration, inhibits intracranial growth in xenograft models of malignant brain tumors with comparable efficacy to AMD 3465. These data indicate that the clinical evaluation of phosphodiesterase inhibitors in the treatment of patients with brain tumors is warranted.
