2. Metabolic Enzyme/Protease PI3K/Akt/mTOR Epigenetics Autophagy Apoptosis
  3. Enolase AMPK Autophagy Apoptosis mTOR Caspase
  4. SU212

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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SU212

SU212 Chemical Structure

CAS No. : 1262219-89-5

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Based on 1 publication(s) in Google Scholar

SU212 Related Antibodies

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Description

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[1][2].

In Vitro

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.

SU212 Related Antibodies

Western Blot Analysis[1]

Cell Line: MDA-MB-231 and EMT6
Concentration: 0.1 μM
Incubation Time: 6 h
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.

Western Blot Analysis[1]

Cell Line: MDA-MB-231 cells
Concentration: 0.5 μM
Incubation Time: 6 h
Result: Did not stabilizes TOP2A.
Induced ENO1 degradation, and this effect was partially rescued by co-treatment with either MG132 or 3MA.

Western Blot Analysis[1]

Cell Line: MDA MB-231, MDA-MB-468, and EMT6
Concentration: 6 h
Incubation Time: 6 or 12 h
Result: Strongly inhibited ENO1 protein expression, does not change ENO3 protein expression.

Cell Proliferation Assay[1]

Cell Line: MDA-MB-231, MDA-MB-468, SUM159 and BT549, 4T1, EMT6, E0771 and PY8119
Concentration: 0.1, 0.25 and 0.5 μM
Incubation Time: 6-10 days
Result: Significantly inhibited TNBC cells’ clono genic potential and eight other cancer types.

Cell Cycle Analysis[2]

Cell Line: MDA-MB-468 and MDA-MB-231
Concentration: 0.1, 0.25 and 0.5 μM
Incubation Time: 6 or 12 h
Result: Increased the sub-g1 phase (20-35%) with 6 h.
Induced mitotic phase arrest (20-31%) with 6 h.

Western Blot Analysis[2]

Cell Line: MDA-MB-468 and MDA-MB-231
Concentration: 0.5 μM
Incubation Time: 6 h
Result: Resulted in the downregulation of cyclin B1 and CDK1 expression, and an increase in the expression of phospho-histone H3.

Western Blot Analysis[2]

Cell Line: MDA-MB-468 and MDA-MB-231
Concentration: 0.5 μM
Incubation Time: 12 h
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.

Western Blot Analysis[2]

Cell Line: MDA-MB-468, MDA-MB-231
Concentration: 0.5 μM
Incubation Time: 6 h
Result: Downregulated of mtor and acetyl-coa carboxylase (ACC) inhibition.

Western Blot Analysis[2]

Cell Line: Dorsomorphin (HY-13418A) pretreated MDA-MB-468 and MDA-MB-231.
Concentration: 0.5 μM
Incubation Time: 6 h
Result: Did not induce AMPK Were healthier and had a morphology similar.

Cell Viability Assay[2]

Cell Line: Dorsomorphin pretreated MDA-MB-468 and MDA-MB-231
Concentration: 0.5 μM
Incubation Time: 72 h
Result: Reverted cytotoxic effect by Dorsomorphin from 73% to 86%.

Cell Viability Assay[2]

Cell Line: MDA-MB-468
Concentration: 0.2, 0.4 and 0.6μM
Incubation Time: 48 h
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).
Parmacokinetics
Species Dose Route T1/2 Cmax Tmax AUC0-t AUC0-∞
Mice[1] 50 mg/kg i.p. 5.2 h 1043 ng/mL 1.00 h 2495 ng·h/mL 2541 ng·h/mL
Rat[1] 50 mg/kg i.p. 8.61 h 915 ng/mL 0.25 h 2781 ng·h/mL 3381 ng·h/mL
In Vivo

SU212 (30 mg/kg, i.p., once daily for 3 days) reduces cellular glycolytic rate, lowering the overall glucose demand of tumor cells in MDA-MB-231 cells induced- female NSG mice[1].
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.

Animal Model: MDA-MB-231 cells induced- female NSG mice (8-9 weeks)[1]
Dosage: 30 mg/kg
Administration: i.p., once daily for 3 days
Result: Did not significantly reduce tumor size compared to the control.
Significantly reduced fdg uptake by tumor cells.
Animal Model: Female C57BL/6 mice and SD rats[1]
Dosage: 100, 200, and 400 mg/kg
Administration: i.p., once
Result: Observed no signs of stress (behavioral, neurological, and auto nomic stresses.
Did not observe any significant weight loss or mortality.
Animal Model: EMT6 cells (1x105) induced-Balb/c mice and PY8119 induced-C57BL/6mice [1]
Dosage: 30 mg/kg
Administration: i.p. 5 days a week for 21 days (EMT6 induced-Balb/c mice) or 24 days (PY8119 induced-C57BL/6mice)
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.
Animal Model: EMT6 cells (1x105) induced-female NSG mice[1]
Dosage: 30 mg/kg
Administration: i.p., 5 days/week for 21 days
Result: Reduced 66% lung metastasis.
Animal Model: Female FVB/N-Tg (MMTV-PyVT) 634 Mul/Jmice (5-6 weeks)[1]
Dosage: 20 mg/kg
Administration: i.p., five days a week
Result: Improved overall survival and reduced tumor burden and incidence.
Animal Model: PY8119 cells (1x105)induced-female Db/Db mice(10 weeks old)[2]
Dosage: 10 mg/kg
Administration: i.p., 5 days/week for 32 days
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.
Animal Model: MDA-MB-231 cells (2× 106) induced-female NOD/SCID mice (7-8 weeks)[2]
Dosage: 15 and 30 mg/kg
Administration: i.p., 21 days
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.
Animal Model: MDA-MB-231 cells (1× 106) induced-female NOD/SCID mice (6-7 weeks)[2]
Dosage: 30 mg/kg
Administration: i.p., every day for 4 weeks
Result: Reduced the number of metastatic foci in the lung by 69%.
Animal Model: 4T1 cells (5×105) induced-female Balb/c mice (7-8 weeks)[2]
Dosage: 30 mg/kg
Administration: i.p., 30 days
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%..
Molecular Weight

437.48

Formula

C25H27NO6
CAS No.
Appearance

Solid

Color

Off-white to gray

SMILES

COC1=CC(C2C3=CC4=C(CCC4)C=C3N(C5=C2C(OC5)=O)CCO)=CC(OC)=C1OC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

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)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.2858 mL 11.4291 mL 22.8582 mL
5 mM 0.4572 mL 2.2858 mL 4.5716 mL
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* 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.

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Purity & Documentation
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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
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SU2121262219-89-5SU 212SU-212EnolaseAMPKAutophagyApoptosismTORCaspasePhosphopyruvate hydrataseAMP-activated protein kinaseMammalian target of RapamycinENO1apoptosisproteasomalautophagicdiabeticfatty livertriple-negative breast cancerInhibitorinhibitorinhibit

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