| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C21H19N5O2S |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
KY386 inhibits the DHX33 helicase with an IC50 of 0.019 μM and reduces the viability of various cancer cells. It induces ferroptosis in cancer cells and apoptosis in some cancer cell lines, increasing intracellular ROS, LPO and Fe2+ while decreasing GSH, and it inhibits growth of gastric and colon cancer xenografts in nude mice. It is applicable to research on liver, lung, pancreatic, colorectal, gastric, breast, renal, prostate, esophageal and cervical cancer, leukemia, glioblastoma and melanoma[1][2]. It is supplied as a white to off-white solid (C21H19N5O2S, MW 405.47) at 99.86% purity.
Physical & Chemical Properties
| CAS Number | 2787598-01-8 |
|---|---|
| Molecular Formula | C21H19N5O2S |
| Molecular Weight | 405.47 g/mol |
| Purity | 99.86% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | COC1=CC=C2N=C(NC2=C1)NC(C3=C(N(C(C)=C3)C4=C(C=C(S4)C)C#N)C)=O |
| Target | Helicase |
| Signaling Pathway | Cell Cycle/DNA Damage; Apoptosis; Metabolic Enzyme/Protease; Immunology/Inflammation; NF-κB |
| Solubility | In Vitro: DMSO: 100 mg/mL (246.63 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. In solvent: -80°C, 6 months; -20°C, 1 month. |
| 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 | 100 mg/mL (246.63 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); 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% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.17 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
KY386 (0-640 nM; 60 min) potently and selectively inhibits helicase activity of recombinant wild-type DHX33 protein, giving an IC50 of 0.019 μM[1]. In U251-MG cancer cells overexpressing DHX33, KY386 (5 nM-20 μM; 48 h) potently inhibits viability, with an IC50 of 0.02 μM[1]. KY386 (72 h) shows broad nanomolar anticancer activity against most of these cell lines: DU145, HCT-116, HepG2, K-562, LoVo, MDA-MB-231, MIA PaCa-2, PC-3 as well as SK-BR-3, NCI-H1299, NCI-H1975, HCC1806, SNU-1, BT549, HCT-15, U-937 as well as A-498, KYSE-150, A549, Daudi, Jurkat T, SNU-387, SW480, Caki-1 as well as SNU-423, CALU-1, COLO 829, T84, U-87MG, NCI-N87, MeWo, HEEC, HGC27 and SGC7901[2]. KY386 (72 h) inhibits viability of the human cancer cell lines A875, A375, T24, 5637, SGC7901, HGC27, and SNU668, with IC50 values between 13 nM (A375) and 35 nM (A875)[2]. KY386 (0-500 nM; 24-72 h) potently induces apoptosis in HuH-7 hepatocellular carcinoma cells and HCT116 colorectal cancer cells in a dose- and time-dependent manner[2]. KY386 (0-50 nM; 4-24 h) raises intracellular ROS levels dose- and time-dependently across many human cancer cell lines (HGC27, 5637, T24, A375, A875, DU145, PC3, and SNU668)[2]. In HGC27 gastric cancer cells, KY386 (0-40 nM; 8-16 h) lowers intracellular GSH levels in a dose- and time-dependent manner[2]. In HGC27, 5637, DU145 and A875 human cancer cells, KY386 (0-60 nM; 8-16 h) raises intracellular LPO levels dose- and time-dependently[2]. KY386 (0-60 nM; 16 h) raises intracellular Fe2+ levels in a dose-dependent manner in 5637, HGC27, DU145, PC3 and SNU668 human cancer cells[2]. In the human cancer cell lines HGC27, 5637, A875, PC-3 and SNU668, KY386 (0-50 nM; 24 h) reduces protein expression of the lipid metabolism-related factors FADS1, FADS2 and SCD1, while having minimal effects on the ferroptosis-related factors GPX4, SLC3A2 and SLC7A11[2]. KY386 (0-40 nM; 0-8 h) downregulates FADS1, FADS2 and SCD1 mRNA levels in a dose-dependent manner in the human cancer cell lines A875, A375, HGC27, T24 and DU145[2].
Cell Cytotoxicity Assay[1]
| Cell Line | U251-MG DHX33-overexpressing glioblastoma cancer cells |
|---|---|
| Concentration | 5 nM, 10 nM, 25 nM, 50 nM, 100 nM, 250 nM, 500 nM, 1000 nM, 2000 nM, 5000 nM, 10 μM or 20 μM |
| Incubation Time | 48 h |
| Result | Exhibited potent cytotoxicity against U251-MG cells, with an IC50 of 0.02 μM (20 nM). Demonstrated moderate metabolic stability with an intrinsic clearance (CLint) of 22.4 mL/min/mg in human liver microsomes. |
Apoptosis Analysis[2]
| Cell Line | HuH-7, HCT116, HGC27, and DU145 human cancer cell lines |
|---|---|
| Concentration | 20 nM, 100 nM, 500 nM (HuH-7, HCT116); 50 nM, 100 nM, 500 nM (HGC27, DU145, 24 h); 100 nM (HGC27, DU145, 48 h) |
| Incubation Time | 48 h, 72 h (HuH-7, HCT116); 24 h, 48 h (HGC27, DU145) |
| Result | Induced apoptosis in a dose- and time-dependent manner in HuH-7 and HCT116 cells. Did not effectively induce apoptosis in HGC27 and DU145 cells, even with increased dose or treatment time. |
Western Blot Analysis[2]
| Cell Line | HGC27, 5637, A875, PC-3, and SNU668 human cancer cell lines |
|---|---|
| Concentration | 20 nM, 40 nM (HGC27, SNU668); 10 nM, 20 nM, 40 nM (5637); 30 nM, 40 nM (A875); 30 nM, 50 nM (PC-3) |
| Incubation Time | 24 h |
| Result | Reduced protein expression of FADS1, FADS2, and SCD1 in all tested cancer cell lines. Had limited effect on GPX4, SLC3A2, and SLC7A11 expression. |
Real Time qPCR[2]
| Cell Line | A875, A375, HGC27, T24, and DU145 human cancer cell lines |
|---|---|
| Concentration | 40 nM (A875, A375, HGC27, DU145); 20 nM, 40 nM (T24, DU145) |
| Incubation Time | 4 h, 6 h, 8 h (A875, A375, HGC27, DU145); 6 h (T24, DU145) |
| Result | Significantly reduced mRNA levels of FADS1, FADS2, and SCD1 in a time- and dose-dependent manner in all tested cancer cell lines, with statistically significant decreases observed at all specified time points and doses. |
In Vivo
In nude mice, KY386 (25-45 mg/kg; i.p.; twice daily for 2 days, then three times daily for 1 day; 7 days in total) inhibits growth of SNU668 gastric cancer xenografts in a dose-dependent manner[2]. KY386 (i.p.; 15-35 mg/kg on days 0-8 and 25-45 mg/kg on days 9-20; given 2 times daily for 2 consecutive days, then 3 times daily for 1 consecutive day; 21 days in total) significantly inhibits growth of RASG12D-mutated colon cancer patient-derived xenografts in nude mice[2].
| Animal Model | Nude mice (female, 5-week old)[2] |
|---|---|
| Dosage | 25 mg/kg; 35 mg/kg; 45 mg/kg |
| Administration | i.p.; BID×2 + TID×1; 7 days |
| Result | Inhibited tumor growth in a dose-dependent manner. Reduced mean tumor volumes compared to vehicle controls at 21 days post-treatment, with the 45 mg/kg dose showing the greatest inhibition. Caused no significant reduction in mouse body weight, indicating minimal toxicity. |
| Animal Model | Nude mice (female, 8-week old)[2] |
|---|---|
| Dosage | 15 mg/kg (Days 0-8) then 25 mg/kg (Days 9-20); 25 mg/kg (Days 0-8) then 35 mg/kg (Days 9-20); 35 mg/kg (Days 0-8) then 45 mg/kg (Days 9-20) |
| Administration | i.p.; BID×2 + TID×1; 21 days |
| Result | Significantly inhibited tumor growth in the RAS G12D mutant colon cancer PDX model. Reduced mean tumor volumes compared to vehicle controls at 21 days post-treatment. Caused no significant reduction in mouse body weight, indicating minimal toxicity. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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