SU212
Based on 1 Customer Validation
SU212 is a podophyllotoxin-derived ENO1 inhibitor and AMPK activator. SU212 can selectively induce oxidative phosphorylation, reduce glycolysis activity and glucose uptake in tumor cells, and directly bind to ENO1 without affecting these pathways in normal cells. SU212 induces apoptosis and promotes ENO1 degradation via proteasomal and autophagic pathways without inhibiting the catalytic activity. SU212 leads to mitotic arrest and apoptosis in TNBC (triple-negative breast cancer) cells by activating AMPK, demonstrating potent anti-tumor activity in vitro. SU212 inhibits tumor growth and metastasis in syngeneic, xenograft, and diabetic mouse models, exhibiting an excellent safety profile. SU212 can be used in research on t TNBC, diabetes, and fatty liver disease.
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- CAS No.: 1262219-89-5
- 화학식: C25H27NO6
- 분자량:437.48
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보관:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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용액&용해도
- 순도&문서
- References
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Help & FAQs
Biological Activity
SU212 (0.01-850 μM, 48 h) demonstrates lower toxicity and higher potency against TNBC cells (MDA-MB-231) than Etoposide with an IC50 of 0.26 μM; inhibits 50% cell viability in human TNBC cells with IC50s values of 0.1, 0.24, and 0.037 μM for MDA-MB-468, SUM159, and BT549 respectively, and in mouse TNBC cell lines with IC50 values of 0.85, 0.18, 0.039, and 0.31 μM for 4T1, EMT6, E0771, and PY8119[1][2].
SU212 (0.5 μM, 6 h) has a different target than Etoposide in MDA-MB-231 cells and promotes ENO1 degradation through both proteasomal and autophagic pathways; this effect is partially blocked by co-treatment with MG132 or 3MA[1].
SU212 (0.1-10 μM, 3 min-6 h) increases the thermal stability of both ENO1 and ENO3 and stronger interaction with ENO1 cells and exhibits a dose-dependent in multiple TNBC cell lines (MDA-MB-231, MDA-MB-468, and EMT6[1].
SU212 (0.25 or 0.5 μM, 1.5 h) inhibits the overall oxygen consumption rate, extracellular acidification rate, and glycolytic rate in MDA-MB-231, MCF12A, and HEK293 cells, without affecting the glycolytic rate or viability of normal cells[1].
SU212 (0.1-0.5 μM, 6-10 days) inhibits the clonogenic potential, reflecting the suppression of tumor regeneration and recurrence, in TNBC cells[1].
SU212 (0.1-0.5 μM, 6 or 12 h) induces G2-/M-phase arrest in MDA-MB-468 and MDA-MB-231[2].
SU212 (0.5 μM, 12 h) decreases the abundances of different forms of tubulin in MCF10A and MCF12A or TNBC MDA-MB-231 and MDA-MB-468 cell lines[2].
SU212 (0.25 or 0.5 μM, 12-48 h) induces 12-60% apoptotic cell death but not autophagic cell death in MDA-MB-468, MDA-MB-231[2].
SU212 (0.25 or 0.5 μM, 1 h-6 h) activates AMPK via phosphorylation of AMPKα at Thr172 in MDA-MB-231 cell and induces robust activation of AMPKα in MDA-MB-468, MDA-MB-231[2].
SU212 (0.25 μM-0.5 μM, 30 min-6 h) inhibits lactate production and decreases the cellular in MDA-MB-468 and MDA-MB-231, not affect the cellular level of D-glucose, glucose-6-phosphate/fructose-6-phosphate, ATP, citrate, OCR and ECAR α-ketoglutarate in MDA-MB-231 cells[2].
SU212 (0.5 μM, 12 h) significantly increases in the levels of proteins associated with oxidative phosphorylation, decreases the levels of proteins associated with glycolysis and the pentose phosphate pathway in MDA-MB-231 and MDA-MB-468 cell lines but not in normal breast cell lines[2].
SU212 (0.1-0.5 μM, 6 or 72 h) has cytotoxic effect that dependent on AMPK activation in MDA-MB-468 and MDA-MB-231[2].
SU212 (0.2-0.6 μM, 48 h) activates AMPK independent of energy stress in TNBC cell lines[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MDA-MB-231 and EMT6
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Concentration:0.1 μM
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Incubation Time:6 h
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Result:Significantly altered the subcellular localization of eno1, most substantially limiting the membrane-bound pool, while exerting more limited effects on its nuclear and mitochondrial pools.
Induced inhibition of eno1 localization to the cell membrane was partially reversed by co-treatment with MG132 and 3MA.
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Cell Line:MDA-MB-231 cells
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Concentration:0.5 μM
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Incubation Time:6 h
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Result:Did not stabilizes TOP2A.
Induced ENO1 degradation, and this effect was partially rescued by co-treatment with either MG132 or 3MA.
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Cell Line:MDA MB-231, MDA-MB-468, and EMT6
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Concentration:6 h
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Incubation Time:6 or 12 h
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Result:Strongly inhibited ENO1 protein expression, does not change ENO3 protein expression.
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Cell Line:MDA-MB-231, MDA-MB-468, SUM159 and BT549, 4T1, EMT6, E0771 and PY8119
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Concentration:0.1, 0.25 and 0.5 μM
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Incubation Time:6-10 days
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Result:Significantly inhibited TNBC cells’ clono genic potential and eight other cancer types.
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Cell Line:MDA-MB-468 and MDA-MB-231
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Concentration:0.1, 0.25 and 0.5 μM
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Incubation Time:6 or 12 h
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Result:Increased the sub-g1 phase (20-35%) with 6 h.
Induced mitotic phase arrest (20-31%) with 6 h.
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Cell Line:MDA-MB-468 and MDA-MB-231
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Concentration:0.5 μM
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Incubation Time:6 h
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Result:Resulted in the downregulation of cyclin B1 and CDK1 expression, and an increase in the expression of phospho-histone H3.
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Cell Line:MDA-MB-468 and MDA-MB-231
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Concentration:0.5 μM
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Incubation Time:12 h
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Result:Cleaved PARP, Bax, Bcl-2 and CC.
Induced pro-apoptotic Bax expression and inhibited Bcl-2 expres sion, leading to a significant increase in Bax/Bcl-2 ratio.
Induced the cleavage of PARP and caspase 3.
Inhibited Beclin-1 but did not affect LC3 A/B.
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Cell Line:MDA-MB-468, MDA-MB-231
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Concentration:0.5 μM
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Incubation Time:6 h
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Result:Downregulated of mtor and acetyl-coa carboxylase (ACC) inhibition.
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Cell Line:Dorsomorphin (HY-13418A) pretreated MDA-MB-468 and MDA-MB-231.
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Concentration:0.5 μM
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Incubation Time:6 h
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Result:Did not induce AMPK Were healthier and had a morphology similar.
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Cell Line:Dorsomorphin pretreated MDA-MB-468 and MDA-MB-231
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Concentration:0.5 μM
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Incubation Time:72 h
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Result:Reverted cytotoxic effect by Dorsomorphin from 73% to 86%.
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Cell Line:MDA-MB-468
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Concentration:0.2, 0.4 and 0.6μM
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Incubation Time:48 h
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Result:Produced an additive inhibitory effect in hypoglycaemic conditions, resulting in about 20–30% enhanced inhibition (P < 0.05) relative to hyperglycaemic conditions.
Did not affect the cytotoxicity of MDA-MB-468 cells by insulin.
Maintained consistent cytotoxicity across physiological and high insulin levels (1–100 ng/ml) but modestly reduced (by 17%) at a supra-pharmacological concentration (10,000 ng/ml).
SU212 (100-400 mg/kg, i.p., once) has well tolerance in in female C57BL/6 mice and SD rats[1].
SU212 (30 mg/kg, i.p. 5 days a week for 21 days or 24 days) not induce liver or kidney toxicity in syngeneic orthotopic TNBC models[1].
SU212 (20 mg/kg, i.p., five days a week) has positive effect on tumor development and progression in hemizygous MMTV-PyMT transgenic female mouse model[1].
SU212 (30 mg/kg, i.p., 5 days/week for 21 days) leads to altered subcellular localization and impaired moonlighting functions by inducing the degradation of ENO1 in orthotopic EMT6 mouse model of TNBC[1].
SU212 (10 mg/kg, i.p., 5 days/week for 32 days) restrains tumor growth in hyperglycemic and hyperinsulinemic conditions and may help improve diabetic and fatty liver conditions in Lepr db (Db/Db) mouse model[1].
SU212 (15 or 30 mg/kg, i.p., 21 days) inhibits tumour progression in luciferase-labelled MDA-MB-231 xenograft mouse model[2].
SU212 (30 mg/kg, i.p., 30 days) inhibits lung metastasis in tail-vein lung-metastasis mouse model[2].
SU212 (30 mg/kg, i.p., 21 days) demonstrates potent antitumor growth and anti-metastatic activity by activating the AMPK pathway with no significant body weight loss or hepatorenal toxicity, improves lipid metabolism in 4T1 syngeneic mouse xenograft[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:MDA-MB-231 cells induced- female NSG mice (8-9 weeks)[1]
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Dosage:30 mg/kg
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Administration:i.p., once daily for 3 days
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Result:Did not significantly reduce tumor size compared to the control.
Significantly reduced fdg uptake by tumor cells.
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Animal Model:Female C57BL/6 mice and SD rats[1]
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Dosage:100, 200, and 400 mg/kg
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Administration:i.p., once
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Result:Observed no signs of stress (behavioral, neurological, and auto nomic stresses.
Did not observe any significant weight loss or mortality.
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Animal Model:EMT6 cells (1x105) induced-Balb/c mice and PY8119 induced-C57BL/6mice [1]
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Dosage:30 mg/kg
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Administration:i.p. 5 days a week for 21 days (EMT6 induced-Balb/c mice) or 24 days (PY8119 induced-C57BL/6mice)
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Result:Significantly delayed tumor growth in both TNBC models, resulting in significantly lower tumor weight at experiment end.
Did not caused any significant changes in these markers of liver or nephrotoxicity in C57BL/6 mice bearing PY8119 tumors.
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Animal Model:EMT6 cells (1x105) induced-female NSG mice[1]
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Dosage:30 mg/kg
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Administration:i.p., 5 days/week for 21 days
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Result:Reduced 66% lung metastasis.
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Animal Model:Female FVB/N-Tg (MMTV-PyVT) 634 Mul/Jmice (5-6 weeks)[1]
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Dosage:20 mg/kg
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Administration:i.p., five days a week
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Result:Improved overall survival and reduced tumor burden and incidence.
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Animal Model:PY8119 cells (1x105)induced-female Db/Db mice(10 weeks old)[2]
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Dosage:10 mg/kg
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Administration:i.p., 5 days/week for 32 days
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Result:Reduced tumor growth.
Reduced overall tumor burden.
Inhibits eno1 expression.
Did not significantly affect overall mouse body weight.
Did cause a significant drop in blood glucose level.
Significantly reduces the level of AST , ALT, alkaline phosphatase and glutamate dehydroge nase (GLDH).
Significantly reduced liver weight.
Reduced fat-associated space by 80%-90%.
Resulted in a distinct mrna profile, characterized by the downregulation of pi3k pathway genes and the upregulation of mitochondrial respiration pathway genes.
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Animal Model:MDA-MB-231 cells (2× 106) induced-female NOD/SCID mice (7-8 weeks)[2]
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Dosage:15 and 30 mg/kg
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Administration:i.p., 21 days
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Result:Inhibited TNBC tumour growth by 46 and 71%, respectively.
Did not show significant body-weight changes and no stress or pain behaviour.
Had 42 and 81% less tumour weight at 15mg/kg and 30mg/kg doses respectively.
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Animal Model:MDA-MB-231 cells (1× 106) induced-female NOD/SCID mice (6-7 weeks)[2]
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Dosage:30 mg/kg
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Administration:i.p., every day for 4 weeks
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Result:Reduced the number of metastatic foci in the lung by 69%.
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Animal Model:4T1 cells (5×105) induced-female Balb/c mice (7-8 weeks)[2]
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Dosage:30 mg/kg
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Administration:i.p., 30 days
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Result:Inhibited tumour growth by 40% without significant body-weight loss.
Reduced tumour weight by 46%.
Reduced the number of metastatic foci in the lung.
Inhibited the expression of Ki-67 and LDHA Bax and c-Caspase 3.
Causes an inhibition of tumour progression via the AMPK pathway.
Induced the expression of Bax and cleaved caspase 3, consistent with western blot and apoptosis assays.
Did not affect blood glucose, cholesterol, creatinine and BUN, whereas levels of triglycerides and ALP decreased signifi cantly.
Reduced tumour weight by 46%..
Chemical Information
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CAS No. 1262219-89-5
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Appearance Solid
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분자량 437.48
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화학식 C25H27NO6
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Color Off-white to gray
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SMILES
COC1=CC(C2C3=CC4=C(CCC4)C=C3N(C5=C2C(OC5)=O)CCO)=CC(OC)=C1OC
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
용액&용해도
DMSO : 50 mg/mL (114.29 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
순도&문서
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Data Sheet (300 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Tailor D, et al., Malhotra SV. Non-orthosteric inhibition of enolase 1 impedes growth of triple-negative breast cancer. Cell Rep Med. 2025 Nov 18;6(11):102451. [Content Brief]
[2]. Tailor D, et al., Novel Aza-podophyllotoxin derivative induces oxidative phosphorylation and cell death via AMPK activation in triple-negative breast cancer. Br J Cancer. 2021 Feb;124(3):604-615. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.2858 mL | 11.4291 mL | 22.8582 mL | 57.1455 mL |
| 5 mM | 0.4572 mL | 2.2858 mL | 4.5716 mL | 11.4291 mL | |
| 10 mM | 0.2286 mL | 1.1429 mL | 2.2858 mL | 5.7145 mL | |
| 15 mM | 0.1524 mL | 0.7619 mL | 1.5239 mL | 3.8097 mL | |
| 20 mM | 0.1143 mL | 0.5715 mL | 1.1429 mL | 2.8573 mL | |
| 25 mM | 0.0914 mL | 0.4572 mL | 0.9143 mL | 2.2858 mL | |
| 30 mM | 0.0762 mL | 0.3810 mL | 0.7619 mL | 1.9048 mL | |
| 40 mM | 0.0571 mL | 0.2857 mL | 0.5715 mL | 1.4286 mL | |
| 50 mM | 0.0457 mL | 0.2286 mL | 0.4572 mL | 1.1429 mL | |
| 60 mM | 0.0381 mL | 0.1905 mL | 0.3810 mL | 0.9524 mL | |
| 80 mM | 0.0286 mL | 0.1429 mL | 0.2857 mL | 0.7143 mL | |
| 100 mM | 0.0229 mL | 0.1143 mL | 0.2286 mL | 0.5715 mL |
SU212 Related Classifications
HY-179578 Related Classifications
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