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> Pathway Inhibitors>TRPM4 Inhibitor NBA

Pathway Inhibitors

TRPM4 Inhibitor NBA View larger

TRPM4 Inhibitor NBA

AOB12909

CAS 667411-04-3 (Free Acid)

Chemical Name: 4-Chloro-2-(1-naphthyloxyacetamido)benzoic acid ammonium salt (NBA)

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Quantity Discount Table - Order More To Get More Price Discount

QuantitymgUnit Price ($/mg or $/Unit)Final Price
15 $24.65 Total: $123.25
110 $20.88 Total: $208.80
125 $17.69 Total: $442.25
150 $15.08 Total: $754.00
1100 $13.05 Total: $1,305.00

Data sheet

Molecular FormulaC19H17ClN2O4
Molecular Weight372.81
CAS Numbers667411-04-3 (free acid)
Storage Condition0°C (short term), -20°C (long term), desiccated
SolubilityDMSO and Water
Purity98% by HPLC
SynonymTRPM4-IN-2 Ammonium Salt
IUPAC/Chemical Name 4-Chloro-2-(1-naphthyloxyacetamido)benzoic acid ammonium salt

More info

Novel specific TRPM4 inhibitor, blocking TRPM4 currents in HCT116 cells, reducing the viability of Colo205 cells. NBA is an ammonium salt form (more water soluble) of TRPM4-IN-2 (Free Acid).

Mechanism / Binding & SAR (Structure-Activity Relationships)

  1. Binding Site / Mode of Inhibition

    • The precise binding site of NBA on TRPM4 has not yet been definitively mapped, although some recent work aims to identify it. PMC+1

    • One publication (“Identification of a binding site for small-molecule inhibitors …”) indicates that efforts are ongoing to pinpoint where anthranilic acid derivatives (like NBA) bind. 

    • Because NBA is an aryloxyacyl-anthranilic acid derivative, its structural features (a naphthoxy substituent, anthranilic acid core) potentially allow interaction with hydrophobic pockets near the transmembrane domain, though this is speculative. Frontiers+2chimia.ch+2

  2. Potency & Selectivity Compared to Other Inhibitors

    • NBA has an IC₅₀ of ~0.16 µM for TRPM4 inhibition.

    • In comparative studies with other TRPM4 inhibitors (e.g. CBA, LBA), NBA tends to show greater potency (i.e. require lower concentration for inhibition). 

    • In colorectal cancer (CRC) cells (HCT116), NBA, CBA, and LBA were found to almost fully block TRPM4 currents (91.8–98.5%) in the low micromolar range; NBA was the most potent among them. MDPI+1

    • Some inhibition is non-reversible in CRC cells (i.e. washout does not fully restore the current), which suggests either very tight binding or possibly partial inactivation. MDPI

  3. Functional Consequences of Inhibition / Downstream Effects

    • In CRC cell lines, inhibition of TRPM4 by NBA was associated with:

      • Slowed proliferation. MDPI

      • Alteration of cell cycle distribution (increased proportion in G1 phase) at higher doses (e.g. ~50 µM). MDPI

      • Reduced viability in a CRC line (Colo205) that expresses high levels of TRPM4. MDPI

    • However, in some prostate cancer (PCa) cell models (DU145, LNCaP), NBA (and related inhibitors) did not reliably change functional readouts (viability, migration) despite blocking current—presumably because inhibition was incomplete or because TRPM4-mediated current alone is not entirely determinative of those phenotypes in those contexts. ScienceDirect+3MDPI+3PMC+3

  4. Functional / Bioactive Profile

    • Target: TRPM4 (Transient Receptor Potential Melastatin 4) channel

    • Action: Inhibitor — it blocks or suppresses TRPM4 activity

    • Potency: IC₅₀ ≈ 0.16 µM (i.e. fairly potent) 

    • In vitro evidence: At 50 µM, TRPM4-IN-2 can block ~88 ± 9% of endogenous TRPM4 currents in DU145 prostate cancer cells over a 0-500 s exposure period.

    • Research uses: It is used as a tool compound in studies of cancer (notably prostate cancer, colorectal cancer) to explore how TRPM4 influences tumor cell behavior.