1. Cell Cycle/DNA Damage
    Apoptosis
  2. Nucleoside Antimetabolite/Analog
    Apoptosis
  3. Fludarabine phosphate

Fludarabine phosphate (Synonyms: NSC 118218 phosphate)

Cat. No.: HY-B0028 Purity: >99.0%
Handling Instructions

Fludarabine (phosphate) is an analogue of adenosine and deoxyadenosine, which is able to compete with dATP for incorporation into DNA and inhibit DNA synthesis.

For research use only. We do not sell to patients.

Fludarabine phosphate Chemical Structure

Fludarabine phosphate Chemical Structure

CAS No. : 75607-67-9

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Customer Review

Based on 8 publication(s) in Google Scholar

Other Forms of Fludarabine phosphate:

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Description

Fludarabine (phosphate) is an analogue of adenosine and deoxyadenosine, which is able to compete with dATP for incorporation into DNA and inhibit DNA synthesis.

In Vitro

Fludarabine phosphate significantly reduces the cell viability in a dose-dependent manner. Fludarabine phosphate exhibits no effect in all tested concentrations when combined with either PBS or control vector, ACE-GFP. Fludarabine phosphate causes a significant decrease in cell viability for 24 h after exposure to ACE-PNP when compared to PBS and ACE-GFP at concentrations of 2.5, 5 and 10 μg/mL[2].

In Vivo

F-araAMP (100 mg/kg given 15 times, 167 mg/kg given 9 times, or 250 mg/kg given 3 times, i.p.) leads to complete regressions of all tumors and cures of all mice. Parental D54 tumors (i.e. without E. coli PNP) are not sensitive to treatment with F-araAMP. Intratumoral injection of Ad/PNP followed by IT F-araAMP can elicit a substantial regressive effect on otherwise refractory solid tumors in a fashion substantially superior to viral PNP transduction followed by systemic prodrug administration[1]. The comparison of ACE-GFP/fludarabine phosphate with ACE-GFP/PBS demonstrats that fludarabine phosphate alone has no growth inhibitory activity on KU-19-19 tumors[2].

Clinical Trial
Molecular Weight

365.21

Formula

C₁₀H₁₃FN₅O₇P

CAS No.

75607-67-9

SMILES

NC1=C2C(N([[email protected]]3[[email protected]@H](O)[[email protected]](O)[[email protected]@H](COP(O)(O)=O)O3)C=N2)=NC(F)=N1

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : ≥ 100 mg/mL (273.82 mM)

H2O : 5 mg/mL (13.69 mM; Need ultrasonic)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.7382 mL 13.6908 mL 27.3815 mL
5 mM 0.5476 mL 2.7382 mL 5.4763 mL
10 mM 0.2738 mL 1.3691 mL 2.7382 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (6.85 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (6.85 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (6.85 mM); Clear solution

  • 4.

    Add each solvent one by one:  PBS

    Solubility: 20 mg/mL (54.76 mM); Clear solution; Need ultrasonic

  • 5.

    Add each solvent one by one:  phosphate buffer saline

    Solubility: 20 mg/mL (54.76 mM); Clear solution; Need ultrasonic

*All of the co-solvents are provided by MCE.
References
Cell Assay
[2]

Briefly, 2×103 KU-19-19 cells are seeded in each well of 96-well plates and allowed to grow overnight. Cells are then exposed to PBS, ACE-GFP or ACE-PNP for 3 h. Twenty-four hours post-infection, the cells are treated with various concentrations of fludarabine phosphate. After the 24-h incubation, cytotoxicity is determined by using WST-1; 4-[3-(4-iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate. The absorbance value is determined at 450 nm by a microplate reader.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[1]

Mice: Parental and E. coli PNP expressing D54MG (human glioma) tumor cells (2×107 cells) are injected subcutaneously into the flanks of nude mice (nu/nu). D54 tumor cells stably transduced with E. coli PNP are prepared as described previously. Tumors are measured with calipers and an estimate of the weight calculated using the equation, (length × width2)/2=mm3, and converted to mg assuming unit density. Unless stated otherwise, therapeutic drugs and the adenoviral vector expressing E. coli PNP (Ad/PNP), or vehicle controls are injected into D54 tumors in 150 μL volumes by 8 separate injections of approximately 20 μL each in an effort to evenly distribute the administered agent. At least 6 mice are studied in each treatment group. Mice are monitored daily and body weights and tumor dimensions collected twice weekly. T-C (tumor growth delay) is determined as the difference in median days to 2 doublings (median days to 600 mg for the D54 and DU145 (human prostate cancer) analysis) between drug-treated and vehicle-treated groups. For the NIH-H322M (human non-small cell lung cancer) study, because of tumor proliferation characteristics, total growth inhibition (TGI) is used as the evaluation point. TGI is equal to the control group mean delta minus the treated group mean delta divided by the control group mean delta, where delta is the change in tumor weight for each animal between day 36 and day 59. The time to the evaluation point for each animal is used as the end point for the student's t-test, Mann-Whitney rank sum test, or a life table analysis in order to statistically compare growth data between treatment groups. All key results are repeated under similar conditions and findings confirmed. Treatments are initiated when tumors are 250 to 300 mg (appr 1-1.5% of total animal weight).

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References
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Keywords:

FludarabineNSC 118218NSC118218NSC-118218Nucleoside Antimetabolite/AnalogApoptosisInhibitorinhibitorinhibit

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Fludarabine phosphate
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HY-B0028
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