1. Protein Tyrosine Kinase/RTK
    JAK/STAT Signaling
  2. EGFR
  3. Falnidamol

Falnidamol (Synonyms: BIBX 1382)

Cat. No.: HY-10322 Purity: 98.07%
Handling Instructions

Falnidamol (BIBX 1382) is a potent, selective inhibitor of EGFR tyrosine kinase (IC50 = 3 nM); displays > 1000-fold lower potency against ErbB2 (IC50 = 3.4 μM) and a range of other related tyrosine kinases (IC50 > 10 μM).

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

Falnidamol Chemical Structure

Falnidamol Chemical Structure

CAS No. : 196612-93-8

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10 mM * 1 mL in DMSO USD 131 In-stock
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Estimated Time of Arrival: December 31
10 mg USD 211 In-stock
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50 mg USD 726 In-stock
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Customer Review

Based on 3 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Falnidamol purchased from MCE. Usage Cited in: Neuroscience. 2015 Jul 20;304:109-121.

    GluN2B Y1472 phosphorylation in whole-cell lysate is increased after 5 and 10 min of EGF treatment in cultured neurons which could be blocked by BIBX-1382. EGFR activation increases SFK activity and phosphorylation of GluN2B Y1472. (A) Representative Western blot result of whole lysate samples from hippocampal slices treated with 50 ng/mL EGF incubation for 10 min. (B) Western blot of EGFR-treated DIV14 cultured hippocampal neurons with minimum glia composition shows increased phosphorylation of
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    Falnidamol (BIBX 1382) is a potent, selective inhibitor of EGFR tyrosine kinase (IC50 = 3 nM); displays > 1000-fold lower potency against ErbB2 (IC50 = 3.4 μM) and a range of other related tyrosine kinases (IC50 > 10 μM).

    IC50 & Target


    3 nM (IC50)

    In Vitro

    Falnidamol (BIBX 1382) and BIBU1361 are both potent and selective submicromolar inhibitors of the EGFR kinase activity. An IC50 value of 3 nM was determined for both compounds. The potency of these two compounds compares with the one obtained with Iressa, which is a leading EGFR inhibitor in the field. Inhibition of the closest family member, HER2, was 100- to 1000-fold less potent. Furthermore, Falnidamol (BIBX 1382) and BIBU1361 did not inhibit a number of other related tyrosine kinases[1].

    In Vivo

    In nude mice, oral once daily dosing at 10 mg/kg with either Falnidamol (BIBX 1382) or BIBU1361 completely suppressed tumor growth of human A431 xenografts with respective T/C values of 15 and 6% after 2 weeks of treatment[1].

    Clinical Trial
    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

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

    DMSO : ≥ 41 mg/mL (105.71 mM)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.5784 mL 12.8919 mL 25.7838 mL
    5 mM 0.5157 mL 2.5784 mL 5.1568 mL
    10 mM 0.2578 mL 1.2892 mL 2.5784 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: ≥ 1.67 mg/mL (4.31 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Animal Administration

    Animal administration[1]
    Five- to six-week-old athymic NMRI-nu/nu female mice (21-31 g) were inoculated s.c. with 1 × 106 (in 100 μl) A431, FaDu, or HN5 cells into the right flank of the animal. After 7 to 11 days, tumors reached a average volume of 40 to 130 mm3. The mice were randomized and treated daily p.o. with Falnidamol (BIBX 1382), BIBU1361, or vehicle control on the basis of individual weights. Tumors were measured three times a week with calipers, and tumor volumes were calculated by the formula π/6 × length × (width)2. Experimental compounds were prepared in 25% aqueous hydroxypropyl-β-cyclodextrin and administered by intragastral gavage. The administration volume was 10 ml/kg b.wt.

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

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    FalnidamolBIBX 1382BIBX1382BIBX-1382EGFREpidermal growth factor receptorErbB-1HER1Inhibitorinhibitorinhibit

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