ANDS
ANDS (1-Amino-8-naphthol-2,4-disulfonic acid) is an orally active inhibitor of CaMKP (IC50 = 6.4 μM; Ki = 3.6 μM) and CaMKP‑N (IC50 = 6.6 μM). ANDS binds unacetylated p53 and restores p53 activity by disrupting ANP32B-p53 interaction. ANDS inhibits chronic myeloid leukemia (CML) cell proliferation, impairs leukemic stem cells (LSC) function and prolongs survival in CML mouse model while sparing normal progenitor cells. ANDS can be used to study the eradication of LSCs and the overcoming of tyrosine kinase inhibitor (TKI) resistance in CML. ANDS can be used to study breast cancer.
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- CAS No.: 16781-09-2
- Formule: C10H7NNa2O7S2
- Masse moléculaire:363.27
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Stockage:
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Activité biologique
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Chemical Information
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Activité biologique
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CaMKP 6.4 μM (IC50) |
CaMKP 3.6 μM (Ki) |
CaMKP-N 6.6 μM (IC50) |
ANDS (compound 5) (5-40 μM; 4 h) inhibits in vitro ANP32B-p53 interaction in a dose-dependent manner[1].
ANDS (5-100 μM; 1 h) inhibits ANP32B-p53 interaction, enhances p53 thermal stability without affecting ANP32B at 5 μM, induces concentration-dependent p53 stabilization at 48°C, and directly targets p53 in KU812 cells in lysate-based CETSA experiments[1].
ANDS (10 μM; 4 h) specifically precipitates GST-tagged p53-CTD, but not ANP32B, in streptavidin pull-down assays, a finding confirmed in KU812 cells, while biotin-conjugated compound retains its ability to disrupt the ANP32B-p53 interaction[1].
ANDS (5 μM) directly binds to immobilized p53‑CTD (KD = 1.496 μM) and, when pre‑incubated with p53‑CTD at 5 μM, weakens the ANP32B‑LCAR/p53‑CTD interaction (KD increased to 18.59 μM)[1].
ANDS (0-80 μM) inhibits the ANP32B-LCAR/p53-CTD interaction in a dose-dependent manner, with an IC50 of 4.5682 μM[1].
ANDS (250 μM) binding induces extensive conformational rearrangements of p53-CTD and precludes its association with ANP32B[1].
ANDS (0-20 μM; 48 h) reduces the viability of KU812 and K562‑p53 cells in a dose‑dependent manner, with IC50 values of 4.637 μM and 5.654 μM[1].
ANDS (1-50 μM; 48 h) nearly abolishes ANP32B-p53 binding and promotes p53 acetylation at 5 μM in KU812 and K562-p53 cells, while 50 μM is needed to disrupt SET/TAF1β-p53 interaction in KU812 cells, demonstrating greater selectivity for ANP32B-p53[1].
ANDS (5 μM; 48 h) significantly enhances p53 acetylation and transcriptional activity in the presence of ANP32B, similar to the effect of ANP32B ablation alone in KU812 cells[1].
ANDS (5 μM; 4 h) specifically pulls down unacetylated p53 (p53WT and p53KR, but not p53KQ) in K562 cells in streptavidin pull-down assays[1].
ANDS (5 μM; 48 h) competitively prevents the interaction between ANP32B and unacetylated p53, leading to increased p53 acetylation, while showing no significant effect on the SET/TAF1β-p53 complex at this concentration in KU812 and K562-p53 cells[1].
ANDS (5 μM; 48 h) enhances p53 transcriptional activity in K562-p53WT and K562-p53KR cells, but not in K562-p53KQ cells[1].
ANDS (5 μM; 48 h) treatment does not alter ANP32B phosphorylation status or its nuclear localization but specifically disrupted the ANP32B-p53 interaction in the nuclei in KU812 cells[1].
ANDS (5 μM; 2-10 days) inhibits proliferation and promotes apoptosis at 5 μM in ANP32B-wildtype KU812 and K562-p53 cells, whereas ANP32B knockdown in KU812 cells partially reverses these effects[1].
ANDS (5 μM) inhibits the CML cell line proliferation by specifically disrupting the direct interaction between ANP32B and p53[1].
ANDS (0-20 μM; 2-7 days) dose-dependently inhibits growth and colony formation and induces apoptosis in Anp32b+/+ CML cells, but promotes growth and inhibits apoptosis in Anp32b–/– CML cells[1].
ANDS (5-20 μM; 6-48 h) dose- and time-dependently upregulates p-CaMKIIγ levels in both KU812 and K562-p53 cells[1].
ANDS (5 μM; 1-10 days) combined with KN93 (HY-15465) synergistically inhibits growth and promotes apoptosis in ANP32B-proficient KU812 cells, but shows no synergy in ANP32B-deficient KU812 cells, where KN93 only blocks ANDS-induced p-CaMKIIγ upregulation without reversing ANDS-promoted growth and apoptosis inhibition; similar results are obtained in K562-p53 cells[1].
ANDS (5 μM) disrupts ANP32B-p53 binding, inhibits cell growth, and promotes apoptosis in TKI‑resistant KBM5‑T315I cells, with these effects being more pronounced when combined with KN93[1].
ANDS (5 μM; 10 days) combined with KN93 exerts synergistic therapeutic efficacy in all three cases of human CML samples[1].
ANDS (compound 5) (0-10 μM) exhibits potent inhibitory activity against CaMKP and CaMKP-N, with IC50 values of 6.4 μM and 6.6 μM, respectively, and a Ki value of 3.6 μM toward CaMKP, while showing no significant inhibition against PP2C or CaN under the same conditions[2].
ANDS (10 μM; 4 min) can inhibit dephosphorylation of phosphoprotein substrates by CaMKP, as in the case of phosphopeptide substrates[2].
ANDS (10 μM; 6 h) can be effectively incorporated into cells to inhibit CaMKP-N expressed in Neuro2a cells[2].
ANDS (0-30 μM; 22 h) causes a marked reduction in cell migration without significant cytotoxicity, again suggesting that the phosphatase activity of CaMKP is crucial for the regulation of cancer cell motility in MDA-MB-231 cells[3].
ANDS (30 μM; 24 h) is able to inhibit the cellular CaMKP activity in MDA-MB-231 cells, thereby inhibiting the cell migration[3].
ANDS (30 μM) does not inhibit the phosphatase activity of hCaMKP-N(1–559) even at 30 μM, a concentration at which the rat CaMKP was strongly inhibited[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
ANDS (10 mg/kg; i.g.; twice a day; 30 days) suppresses Anp32b⁺/⁺ CML and LSCs while accelerating Anp32b⁻/⁻ CML in both primary and secondary transplanted mice, indicating that ANDS impairs LSC function via ANP32B-p53 disruption but also exerts ANP32B-independent effects[1].
ANDS (10 mg/kg; i.g.; twice a day; 8 days) synergizes with KN93 to suppress CML progression through p‑CaMKIIγ inhibition in Bcr‑AblWT‑induced CML mouse models[1].
ANDS (10 mg/kg; i.g.; twice a day; 8 days) combined with KN93 synergistically suppresses Anp32b⁺/⁺ CML progression in Bcr‑AblWT‑induced CML mouse models, but exhibits no such synergy in Anp32b⁻/⁻ CML mice[1].
ANDS (10 mg/kg; i.g.; twice a day; 8 days) combined with KN93 synergistically suppresses the progression of both TKI-sensitive and -resistant CML in mouse models[1].
ANDS (10 mg/kg; i.g.; twice a day; 8 days) as a single agent is effective, and combined with KN93 exhibits a stronger effect in the Bcr‑AblT315I‑induced Imatinib (HY-15463) ‑resistant CML mouse model[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice[1]
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Dosage:10 mg/kg
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Administration:i.g.; twice a day; 30 days
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Result:Resulted in a slight decrease in the frequencies of Lin–Sca-1+c-Kit+ (LSK) cells, including LT-HSCs, ST-HSCs, and MPPs.
Don’t affect total bone marrow (BM) cell numbers, progenitor and mature cell populations.
Don’t cause significant alterations in body weight or the appearance of the livers, spleens, and lungs.
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Animal Model:10-12-week-old donor mice are injected with 5‑fluorouracil (120 mg/kg) via tail vein; 6 days later, their Lin⁻ bone marrow cells are harvested, infected with Bcr‑AblWT or Bcr‑AblT315I‑IRES‑GFP virus, and then transplanted (5×10⁴ cells) into lethally irradiated (3+3 Gy) C57BL/6 recipients, from which GFP⁺ leukemic cells are subsequently isolated for secondary transplantation into new recipients[1].
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Dosage:10 mg/kg
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Administration:i.g.; twice a day; 8 days
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Result:Showed that the two-agent combinations demonstrated greater efficacy compared to the single agents, while the three-agent combination exhibited the most potent effect.
Decreased counts of GFP+ CML cells in peripheral blood (PB) and BM, reduced GFP+LSK cells, and increased percentage of apoptotic GFP+LSK cells in BM, as well as reduced spleen size and weight and prolonged mouse survival.
Chemical Information
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CAS No. 16781-09-2
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Masse moléculaire 363.27
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Formule C10H7NNa2O7S2
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SMILES
NC1=C(C=C(C2=C1C(O)=CC=C2)S(=O)(O[Na])=O)S(=O)(O[Na])=O
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Synonyms
1-Amino-8-naphthol-2,4-disulfonic acid
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Wei YS, et al. The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia. Nat Commun. 2026 Jun 10. [Content Brief]
[2]. Sueyoshi N, et al. Inhibitors of the Ca(2+)/calmodulin-dependent protein kinase phosphatase family (CaMKP and CaMKP-N). Biochem Biophys Res Commun. 2007 Nov 23;363(3):715-21. [Content Brief]
[3]. Akizuki K, et al. CaMK phosphatase (CaMKP/POPX2/PPM1F) inhibitors suppress the migration of human breast cancer MDA-MB-231 cells with loss of polarized morphology. Biochem Biophys Res Commun. 2023 Jan 8;639:1-8. [Content Brief]
[4]. Ishida A, et al. An active C-terminally truncated form of Ca (2+) /calmodulin-dependent protein kinase phosphatase-N (CaMKP-N/PPM1E). Biomed Res Int. 2013;2013:134813. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
ANDS Related Classifications
HY-184486 Related Classifications
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