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Fig. 1 · Structure
Cat. No.
A10868
CAS No.
18883-66-4
Formula
C8H15N3O7
Mol. Weight
265.2

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Streptozotocin

Cat. No. A10868 CAS 18883-66-4

O-GlcNAcase inhibitor

Streptozotocin (Streptozocin, Zanosar, STZ)is used in medical research to produce an animal model for Type 1 diabetes, which directly inhibist the O-GlcNAcase activity of the enzyme NCOAT in vitro.

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Publications for Streptozotocin

10 publications citing this product

  1. Zhen Liang, .et al. , Nat Metab, 2023, Jan;5(1):29-40 PMID: 36624157
  2. Alemayehu Toma, .et al. , J Exp Pharmacol, 2022, 14: 309-316 PMID: 36317069
  3. Andressa Braga, .et al. , Braz J Pharm Sci, 2022, 58: e19674
  4. Yuanyuan Du, .et al. , Nat Med, 2022, Feb;28(2):272-282 PMID: 35115708
  5. Karemah A. Alatawi, .et al. , Saudi Journal of Biological Sciences, 2021, 25 June PMID: 34354403
  6. D.H. Mhya, .et al. , Asian J Exp Biol Sci, 2019, 12 (2): 164-172
  7. Stanley I. R. Okoduwa, .et al. , J Diabetol, 2017, 8(3): 74-85
  8. Stanley I. R. Okoduwa, .et al. , Medicines (Basel), 2017, Dec; 4(4): 73 PMID: 29019956
  9. Stanley I. R. Okoduwa, .et al. , PLoS One, 2017, 12(1): e0170971 PMID: 28129400
  10. Stanley I. R. Okoduwa, .et al. , World J Diabetes, 2016, Dec 15; 7(20): 605-614 PMID: 28031778
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Biological Activity

Bioactivity / Mechanism

Streptozotocin inhibits human O-GlcNAcase. In a purified-enzyme assay, inhibition was competitive (Ki 64 ± 3 μM), with no increase in inhibition after longer preincubation. In Min6 cells, O-GlcNAcase inhibition and loss of viability were separable in comparator experiments, limiting the use of STZ as a selective probe of O-GlcNAc-dependent cell death. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

GLUT2 expression increased STZ susceptibility in engineered RINm5F cells. The reported MTT EC50 was 25.1 ± 0.4 mmol/l in nontransfected cells and 2.1 ± 0.2 and 3.9 ± 0.3 mmol/l in GLUT2 clones A and B, respectively (mean ± SEM; five experiments). These are model-specific viability endpoints. [2]

Competitive inhibition of human O-GlcNAcase

Biochemical assay · Purified GST-tagged human OGA, residues 53–916 [1]

STZ competitively inhibited human OGA. Longer preincubation did not shift the inhibition curves, arguing against time-dependent irreversible inhibition in this assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Inhibition of human OGA hydrolysis of 4MU-GlcNAcKi 64 ± 3 μM[1]

Literature-Reported Treatment Conditions

Treatment concentration
STZ: 0, 30, 60, 120 μM for Ki determination; varied substrate concentrations (0–250 μM in standard kinetic assays).
Exposure duration
3 min preincubation; 60 min reaction at room temperature for hOGA.
Method
4MU-GlcNAc fluorescence assay; 2 nM hOGA; pH 6.8 McIlvaine buffer with BSA. Zero-STZ kinetic series and background emission corrections.
Vehicle
Water for STZ stock.
Reported limits
No A10868 lot comparison. The uncertainty convention for fitted Ki is not specified.
Methods and source locations

Compound reported in the paper: Streptozotocin; Compound label in the paper: STZ

Reported streptozotocin material only; supplier lot, purity and anomer distribution are not validated for A10868.

Fig.2B–C; Results and Discussion, human OGA kinetics; Experimental Procedures: Enzyme Kinetics

Inhibition of human OGA hydrolysis of 4MU-GlcNAc: Competitive fit of steady-state fluorescence data; 3 min enzyme/inhibitor preincubation followed by 60 min reaction. Experiments in triplicate; the meaning of ± for this fitted Ki is not explicitly specified. — Fig.2C and Results and Discussion; Enzyme Kinetics

O-GlcNAc accumulation and Min6 viability are separable

Cell-based study · Mouse Min6 insulinoma cells [1]

STZ raised O-GlcNAc immunoblot signal at high millimolar concentrations and reduced viability. Gal-STZ also reduced viability without an observable O-GlcNAc increase; GlcNAcstatin strongly raised O-GlcNAc without reducing viability in the tested assay. These controls limit attribution of STZ toxicity to OGA inhibition.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Protein O-GlcNAcylationQualitative immunoblot STZ increased signal; Gal-STZ showed no observable increase; GlcNAcstatin produced a larger increase.[1]
Cell viability relative to untreated cellsTrypan blue viability Both STZ and Gal-STZ decreased viability; GlcNAcstatin did not.[1]

Literature-Reported Treatment Conditions

Treatment concentration
STZ 5 or 10 mM; separate comparator treatments Gal-STZ 5 or 10 mM and GlcNAcstatin 20 μM.
Exposure duration
16 hr immunoblot; 6 hr trypan-blue viability.
Method
Parallel single-agent comparison with untreated controls.
Vehicle
STZ/Gal-STZ dissolved in culture medium; GlcNAcstatin stock in DMSO.
Co-treatment
None; comparator agents were separate treatments.
Reported limits
Independent biological replicate count is not distinguished from triplicate measurements. A matched DMSO-only control is not identified in Fig.3. No universal OGA toxicity conclusion is inferred.
Methods and source locations

Compound reported in the paper: Streptozotocin; Compound label in the paper: STZ

Reported streptozotocin material only; supplier lot, purity and anomer distribution are not validated for A10868.

Fig.3A–B and captions; Results and Discussion; Min6 culture, western blotting and cell viability methods

Protein O-GlcNAcylation: Anti-O-GlcNAc CTD110.6 western blot with β-tubulin loading panel; 16 hr treatment. — Fig.3A and caption

Cell viability relative to untreated cells: 6 hr treatment; live cells measured in triplicate; untreated = 100%. Caption describes errors as standard deviation of the mean. No precise percentages taken from bars. — Fig.3B and caption; Cell Viability Assays

GLUT2 expression changes susceptibility to STZ

Cell-based study · Rat RINm5F insulin-producing cells, nontransfected controls, glucokinase clone and GLUT2 clones A/B [2]

GLUT2-expressing clones were more susceptible to STZ than nontransfected or glucokinase-expressing controls. GLUT2 did not comparably enhance toxicity of the four other alkylating agents tested, supporting transporter-associated selectivity rather than a generic increase in susceptibility.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
STZ concentration causing 50% loss of MTT viability in Nontransfected RINm5FEC50 25.1 ± 0.4 mmol/l (5)[2]
STZ concentration causing 50% loss of MTT viability in RINm5F-GKEC50 20.5 ± 0.3 mmol/l (5)[2]
STZ concentration causing 50% loss of MTT viability in RINm5F-GLUT2-AEC50 2.1 ± 0.2 mmol/l (5)[2]
STZ concentration causing 50% loss of MTT viability in RINm5F-GLUT2-BEC50 3.9 ± 0.3 mmol/l (5)[2]

Literature-Reported Treatment Conditions

Treatment concentration
Concentration-response series; Fig.3 displays 0–20 mmol/l STZ. EC50 estimates are fitted assay endpoints, not treatment recommendations.
Exposure duration
1 hr compound exposure, followed by 18 hr in RPMI 1640 before MTT viability measurement.
Method
MTT signal expressed as percentage of untreated cells; GLUT2 expression verified by Northern/Western blot. Glucokinase clone and MNU/ENU/MMS/EMS serve as specificity controls.
Vehicle
Test compounds dissolved in 10 mmol/l HCl immediately before addition to glucose-free HEPES-supplemented Krebs–Ringer bicarbonate medium.
Reported limits
Anomer composition and lot-specific purity not specified; no direct DNA-adduct measurement adopted.
Methods and source locations

Compound reported in the paper: Streptozotocin; Compound label in the paper: STZ

Reported streptozotocin material only; supplier lot, purity and anomer distribution are not validated for A10868.

pp.1529–1532; Figs.2–4 and Table 1; Tissue culture and viability tests

STZ concentration causing 50% loss of MTT viability in Nontransfected RINm5F: Mean ± SEM; parentheses indicate number of experiments. Nonlinear regression; both GLUT2 clones p < 0.01 versus nontransfected control. — Table 1, STZ row and footnote; Fig.3

STZ concentration causing 50% loss of MTT viability in RINm5F-GK: Mean ± SEM; parentheses indicate number of experiments. Nonlinear regression; both GLUT2 clones p < 0.01 versus nontransfected control. — Table 1, STZ row and footnote; Fig.3

STZ concentration causing 50% loss of MTT viability in RINm5F-GLUT2-A: Mean ± SEM; parentheses indicate number of experiments. Nonlinear regression; both GLUT2 clones p < 0.01 versus nontransfected control. — Table 1, STZ row and footnote; Fig.3

STZ concentration causing 50% loss of MTT viability in RINm5F-GLUT2-B: Mean ± SEM; parentheses indicate number of experiments. Nonlinear regression; both GLUT2 clones p < 0.01 versus nontransfected control. — Table 1, STZ row and footnote; Fig.3

In Vivo Studies

In male C57BL/6J mice, STZ-induced hyperglycemia coexisted with substantial remaining insulin-positive β-cell volume and no significant difference in total islet numbers versus controls. Whole-pancreas imaging showed that the extent and timing of volume loss depended on the regimen; elevated blood glucose alone did not establish complete β-cell ablation. [3]

Hyperglycemia with retained pancreatic β-cell volume

Animal study · Male C57BL/6J mice; whole-pancreas insulin-labelled optical projection tomography [3]

Hyperglycemia occurred after either STZ regimen despite substantial remaining insulin-positive β-cell volume. SHD reduced volume at weeks 1 and 2; MLD showed a significant reduction only at week 1. Total islet numbers did not differ significantly at the sampled times. Hyperglycemia cannot be treated as evidence of complete β-cell ablation in this model.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Blood glucose after STZHyperglycemia criterion >12 mmol/L[3]
Whole-pancreas insulin-positive β-cell volumeReported significance SHD: p = 0.008 (week 1), p = 0.0014 (week 2); MLD: p = 0.0078 (week 1).[3]
Whole-pancreas islet numberComparison with untreated control No significant differences at weeks 1–3 in either regimen.[3]

Conditions shared by the study groups

Route
Intraperitoneal
Vehicle
0.1 M sodium citrate buffer, pH 4.5
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Single high dose
150 mg/kg		Untreated controls for OPT; separate vehicle controls examined in SI Fig.2.Hyperglycemia and significant reduction in insulin-positive volume at weeks 1–2; no significant change in total islet number.[3]
Multiple low doses
50 mg/kg		Untreated controls for OPT; separate vehicle controls examined in SI Fig.2.Hyperglycemia developed later; no elevated glucose at week 1. Significant volume reduction at week 1 only; total islet number unchanged.[3]
Single high dose
Model: Male C57BL/6J mice
Frequency: Once
Treatment course: Single administration; assessed 1–3 weeks later
Reported limits: Age not specified for this experiment in the read main-text methods.
Multiple low doses
Model: Male C57BL/6J mice
Frequency: Once daily
Treatment course: 5 consecutive days; assessed 1–3 weeks after first administration
Reported limits: Age not specified for this experiment in the read main-text methods.
Methods and source locations

Compound reported in the paper: Streptozotocin; Compound label in the paper: STZ

Reported streptozotocin material only; supplier lot, purity and anomer distribution are not validated for A10868.

Fig.2a–c and caption; Results, whole-pancreas OPT comparison; Methods: Mice, Organ processing and optical projection tomography, Statistics; SI Fig.2

Blood glucose after STZ: Glucose measurements at weeks 0–3. No MLD-treated animal had elevated glucose at week 1. Fig.2a n=15,15,10,5 at weeks 0,1,2,3; error bars SEM. — Fig.2a and caption; Results paragraph beginning To corroborate

Whole-pancreas insulin-positive β-cell volume: OPT volumetry; untreated controls. Controls n=5 per time; SHD n=3,4,3 and MLD n=5,4,3 at weeks 1,2,3; SEM. Two-way ANOVA with Tukey post hoc comparisons. No volumes estimated from bars. — Fig.2b and caption; associated Results; Statistics

Whole-pancreas islet number: Same pancreata and sample sizes as Fig.2b; not an independent experiment. Vehicle-versus-untreated comparison in SI Fig.2 supports control choice. — Fig.2c; associated Results; SI Fig.2

Single high dose · Fig.2a–c and caption; Results, whole-pancreas OPT comparison; Methods: Mice, Organ processing and optical projection tomography, Statistics; SI Fig.2

Multiple low doses · Fig.2a–c and caption; Results, whole-pancreas OPT comparison; Methods: Mice, Organ processing and optical projection tomography, Statistics; SI Fig.2

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 18883-66-4
Applications O-GlcNAcase inhibitor
Formula C8H15N3O7
Molecular Weight 265.2
Synonyms Streptozocin; Zanosar; STZ
SMILES
CN(C(=O)N[C@@H]1[C@H]([C@@H]([C@H](O[C@@H]1O)CO)O)O)N=O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 51 mg/mL (192.29 mM)
Water 51 mg/mL (192.29 mM)
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
Saline

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Pathak S, Dorfmueller HC, Borodkin VS, et al. Chemical dissection of the link between streptozotocin, O-GlcNAc, and pancreatic cell death. Chemistry & biology (2008). PMID: 18721751 DOI: 10.1016/j.chembiol.2008.06.010 Source material
  2. [2] Elsner M, Guldbakke B, Tiedge M, et al. Relative importance of transport and alkylation for pancreatic beta-cell toxicity of streptozotocin. Diabetologia (2000). PMID: 11151762 DOI: 10.1007/s001250051564 Source material
  3. [3] Hahn M, van Krieken PP, Nord C, et al. Topologically selective islet vulnerability and self-sustained downregulation of markers for β-cell maturity in streptozotocin-induced diabetes. Communications biology (2020). PMID: 32999405 DOI: 10.1038/s42003-020-01243-2 Source material

Publications

10 publications citing this product

  1. Zhen Liang, .et al. , Nat Metab, 2023, Jan;5(1):29-40 PMID: 36624157
  2. Alemayehu Toma, .et al. , J Exp Pharmacol, 2022, 14: 309-316 PMID: 36317069
  3. Andressa Braga, .et al. , Braz J Pharm Sci, 2022, 58: e19674
  4. Yuanyuan Du, .et al. , Nat Med, 2022, Feb;28(2):272-282 PMID: 35115708
  5. Karemah A. Alatawi, .et al. , Saudi Journal of Biological Sciences, 2021, 25 June PMID: 34354403
  6. D.H. Mhya, .et al. , Asian J Exp Biol Sci, 2019, 12 (2): 164-172
  7. Stanley I. R. Okoduwa, .et al. , J Diabetol, 2017, 8(3): 74-85
  8. Stanley I. R. Okoduwa, .et al. , Medicines (Basel), 2017, Dec; 4(4): 73 PMID: 29019956
  9. Stanley I. R. Okoduwa, .et al. , PLoS One, 2017, 12(1): e0170971 PMID: 28129400
  10. Stanley I. R. Okoduwa, .et al. , World J Diabetes, 2016, Dec 15; 7(20): 605-614 PMID: 28031778

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