| Field | Specification |
|---|---|
| Target | |
| Alternative names | CID-49852229 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C15H9F4N5OS |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
ML216, also known as CID-49852229, is a potent, selective, and cell-permeable inhibitor of the DNA-unwinding activity of BLM helicase, with IC50 values of 2.98 μM and 0.97 μM for BLM full-length and BLM 636-1298, respectively. It also inhibits the ssDNA-dependent ATPase activity of BLM, with a Ki of 1.76 μM, and it exhibits antitumor activity[1][2]. It is supplied as a light yellow to yellow solid (C15H9F4N5OS, MW 383.32) at 99.89% purity.
Physical & Chemical Properties
| CAS Number | 1430213-30-1 |
|---|---|
| Molecular Formula | C15H9F4N5OS |
| Molecular Weight | 383.32 g/mol |
| Purity | 99.89% |
| Appearance | Solid |
| Color | Light yellow to yellow |
| SMILES | O=C(NC1=CC=C(F)C(C(F)(F)F)=C1)NC2=NN=C(S2)C3=CC=NC=C3 |
| Target | Helicase |
| Signaling Pathway | Cell Cycle/DNA Damage |
| Solubility | In Vitro: DMSO: 20 mg/mL (52.18 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 20 mg/mL (52.18 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | 2 mg/mL (5.22 mM); suspension; requires sonication |
| How to prepare | Gives a suspension at 2 mg/mL. The suspension is suitable for oral and intraperitoneal dosing. For 1 mL of working solution: add 100 μL DMSO stock (20.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Data provided by the manufacturer.
In Vitro
Treatment with ML216 (12.5-50 μM; 24-72 hours; PSNG5 and PSNG13 cells) suppresses PSNF5 cell proliferation concentration-dependently, with no such effect on PSNG13 cells[1]. In PSNF5 cells, ML216 significantly raises the frequency of sister chromatid exchanges (SCEs), while PSNG13 cells show no such increase[1]. Sensitivity of PSNF5 cells to aphidicolin is increased by ML216, whereas isogenic PSNG13 cells lacking BLM are not sensitized[1]. ML216 inhibits both full length WRN (IC50 of 5 μM) and a truncated WRN500-946 (IC50 of 12.6 μM); the full-length form is 2.5-fold more sensitive. BLM is slightly more sensitive than WRN to ML216 inhibition (1.7-fold based on IC50 values). Even though ML216 detectably inhibits WRN, the compound appears selective for BLM in human cells. Proliferation of WRN+ and WRN cells is inhibited equally well by ML216, which also sensitizes both cell types to aphidicolin similarly[1].
Cell Proliferation Assay[1]
| Cell Line | PSNG5 and PSNG13cells |
|---|---|
| Concentration | 12.5 μM or 50 μM |
| Incubation Time | 24 hours, 48 hours, 72 hours |
| Result | Inhibited the proliferation of PSNF5 cells, but not of PSNG13 cells, and did so in a concentration-dependent manner. |
In Vivo
ML216 inhibits unwinding by the sequence-related BLM and WRN helicases to a similar degree in vitro; however, the apparent reliance on BLM for ML216 to produce biological effects in human cells points to BLM specificity in the mechanism of action of the drug in vivo. A co-crystal structure of BLM bound to the inhibitor would be informative. In vivo, cellular cues may induce a specific WRN conformation that resists ML216[2].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Targeting BRCA1-deficient PARP inhibitor-resistant cells with nickases reveals nick resection as a cancer vulnerability. Nat Cancer 2025 Feb;6(2):278-291. PMID: 39838098
Synergistic protection of nascent DNA at stalled forks by MSANTD4 and BRCA1/2-RAD51. Nat Chem Biol 2025 Aug;21(8):1182-1193. PMID: 39809895
PARP1 negatively regulates transcription of BLM through its interaction with HSP90AB1 in prostate cancer. J Transl Med 2023 Jul 6;21(1):445. PMID: 37415147
Genomic context influences translesion synthesis DNA polymerase-dependent mechanisms of micronuclei induction by G-quadruplexes. Cell Rep 2025 May 10;44(5):115706. PMID: 40349342
LIG1 Loss in TP53-mutant Triple Negative Breast Cancer Rewires DNA Repair and Confers Sensitivity to PARP-ATR Inhibitor Combinations. Mol Cancer Ther 2026 Jul 15:10.1158/1535-7163.MCT-26-0182. PMID: 42456172
ML216 Prevents DNA Damage-Induced Senescence by Modulating DBC1-BLM Interaction. Cells 2022 Dec 29;12(1):145. PMID: 36611939
ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway. Int J Mol Sci 2026 Apr 10;27(8):3425. PMID: 42074068
BLM interaction with EZH2 regulates MDM2 expression and is a poor prognostic biomarker for prostate cancer. Am J Cancer Res 2021 Apr 15;11(4):1347-1368. PMID: 33948362
Utrecht University. 2023 Feb.
