Systematic (IUPAC) name
Clinical data
AHFS/ Micromedex Detailed Consumer Information
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Pharmacokinetic data
Half-life 10.4 hours
CAS number 21187-98-4 
ATC code A10BB09
PubChem CID 3475
DrugBank DB01120
ChemSpider 3356 
KEGG D01599
ChEBI CHEBI:31654 
Chemical data
Formula C15H21N3O3S
Mol. mass 323.412 g/mol
SMILES O=S(=O)(c1ccc(cc1)C)NC(=O)NN3CC2CCCC2C3
InChI InChI=1S/C15H21N3O3S/c1-11-5-7-14(8-6-11)22(20,21)17-15(19)16-18-9-12-3-2-4-13(12)10-18/h5-8,12-13H,2-4,9-10H2,1H3,(H2,16,17,19)

Gliclazide is an oral hypoglycemic (anti-diabetic drug) and is classified as a sulfonylurea.Its classification has been ambiguous, as literature uses it as both a first- generation[1] and second-generation[2] sulfonylurea. Gliclazide was shown to protect human pancreatic beta-cells from hyperglycemia-induced apoptosis.[3] It was also shown to have an antiatherogenic effect (preventing accumulation of fat in arteries) in type 2 diabetes.[4]

Form and composition

Each immediate-release tablet contains 80 mg. Modified release formulations contain 30 mg and 60 mg of gliclazide


Gliclazide is used for control of hyperglycemia in gliclazide-responsive diabetes mellitus of stable, mild, non-ketosis prone, type 2 diabetes. It is used when diabetes cannot be controlled by proper dietary management and exercise or when insulin therapy is not appropriate.National Kidney Foundation (2012 Update) claims that Gliclazide doesn’t requires dosage uptitration even in end stage Kidney disease.

Mode of action

Gliclazide selectively binds to sulfonylurea receptors (SUR-1) on the surface of the pancreatic beta-cells. It was shown to provide cardiovascular protection as it does not bind to sulfonylurea receptors (SUR-2A) in the heart.[5] This binding effectively closes the K+ ion channels. This decreases the efflux of potassium from the cell which leads to the depolarization of the cell. This causes voltage dependent Ca++ ion channels to open increasing the Ca++ influx. The calcium can then bind to and activate calmodulin which in turn leads to exocystosis of insulin vesicles leading to insulin release.


The dosage for the 80 mg formulation is 40 to 320 mg daily in two divided doses, while the 30 mg and 60 mg modified release formulation may be given at a dose of 30 to 120 mg once daily at breakfast.


Water Solubility = 0.027 mg/L[6]

  • Hypoglycemic sulfonylurea, restoring first peak of insulin secretion, increasing insulin sensitivity.
  • Glycemia-independent hemovascular effects, antioxidant effect.
  • No active circulating metabolites.


  • Type 1 diabetes
  • Hypersensitivity to sulfonylureas
  • Severe renal or hepatic failure
  • Pregnancy and lactation
  • Miconazolecoprescription


Gliclazide undergoes extensive metabolism to several inactive metabolites in humans, mainly methylhydroxygliclazide and carboxygliclazide. CYP2C9 is involved in the formation of hydroxygliclazde in human liver microsomes and in a panel of recombinant human P450sin vitro.[7][8] But the pharmacokinetics of gliclazide MR are affected mainly by CYP2C19 genetic polymorphism instead of CYP2C9 genetic polymorphism.[9][10]


Hyperglycemic action may be caused by danazolchlorpromazineglucocorticoidsprogestogens, or β-2 agonists. Its hypoglycemic action may be potentiated by phenylbutazone, alcohol, fluconazole, β-blockers, and possibly ACE inhibitors. It has been found that rifampin increases gliclazide metabolism in humans in vivo.[11]

Adverse effects

  • Hypoglycemia– while it was shown to have the same efficacy as glimepiride, one of the newer sulfoylureas, the European GUIDE study has shown that it has approximately 50% fewer confirmed hypoglycaemic episodes in comparison with glimepiride.[12]
  • Gastrointestinal disturbance (reported)
  • Skin reactions(rare)
  • Hematological disorders (rare)
  • Hepatic enzyme rises (exceptional)

Adverse effects

Gliclazide overdose may cause severe hypoglycemia, requiring urgent administration of glucose by IV and monitoring.


  1. ^Ballagi-Pordány, György; Köszeghy, Anna; Koltai, Mária-Zsófia; Aranyi, Zoltán; Pogátsa, Gábor (1990). “Divergent cardiac effects of the first and second generation hypoglycemic sulfonylurea compounds”. Diabetes Research and Clinical Practice 8 (2): 109–14.doi:1016/0168-8227(90)90020-TPMID 2106423.
  2. ^Shimoyama, Tatsuhiro; Yamaguchi, Shinya; Takahashi, Kazuto; Katsuta, Hidenori; Ito, Eisuke; Seki, Hiroyuki; Ushikawa, Kenji; Katahira, Hiroshi et al. (2006). “Gliclazide protects 3T3L1 adipocytes against insulin resistance induced by hydrogen peroxide with restoration of GLUT4 translocation”. Metabolism 55 (6): 722–30. doi:1016/j.metabol.2006.01.019PMID 16713429.
  3. ^Del Guerra, S; Grupillo, M; Masini, M; Lupi, R; Bugliani, M; Torri, S; Boggi, U; Del Chiaro, M et al. (2007). “Gliclazide protects human islet beta-cells from apoptosis induced by intermittent high glucose”. Diabetes/Metabolism Research and Reviews 23 (3): 234–8.doi:1002/dmrr.680PMID 16952202.
  4. ^Katakami, N.; Yamasaki, Y.; Hayaishi-Okano, R.; Ohtoshi, K.; Kaneto, H.; Matsuhisa, M.; Kosugi, K.; Hori, M. (2004). “Metformin or gliclazide, rather than glibenclamide, attenuate progression of carotid intima-media thickness in subjects with type 2 diabetes”.Diabetologia 47 (11): 1906–13. doi:1007/s00125-004-1547-8PMID 15565373.
  5. ^Lawrence, C. L.; Proks, P.; Rodrigo, G. C.; Jones, P.; Hayabuchi, Y.; Standen, N. B.; Ashcroft, F. M. (2001). “Gliclazide produces high-affinity block of K ATP channels in mouse isolated pancreatic beta cells but not rat heart or arterial smooth muscle cells”.Diabetologia 44 (8): 1019–25. doi:1007/s001250100595PMID 11484080.
  6. ^Gopal Venkatesh Shavi et al. Enhanced dissolution and bioavailability of gliclazide using solid dispersion techniques; International Journal of Drug Delivery 2 (2010) 49-57
  7. ^Rieutord, A; Stupans, I; Shenfield, GM; Gross, AS (1995). “Gliclazide hydroxylation by rat liver microsomes”. Xenobiotica 25 (12): 1345–54. doi:3109/00498259509061922PMID 8719909.
  8. ^Elliot, David J.; Lewis, Benjamin C.; Gillam, Elizabeth M. J.; Birkett, Donald J.; Gross, Annette S.; Miners, John O.; Miners, JO (2007). “Identification of the human cytochromes P450 catalysing the rate-limiting pathways of gliclazide elimination”British Journal of Clinical Pharmacology 64 (4): 450–7. doi:1111/j.1365-2125.2007.02943.xPMC 2048545PMID 17517049.
  9. ^Zhang, Yifan; Si, Dayong; Chen, Xiaoyan; Lin, Nan; Guo, Yingjie; Zhou, Hui; Zhong, Dafang (2007). “Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects”British Journal of Clinical Pharmacology 64(1): 67–74. doi:1111/j.1365-2125.2007.02846.xPMC 2000619PMID 17298483.
  10. ^Xu, H; Williams, K M; Liauw, W S; Murray, M; Day, R O; McLachlan, A J (2009). “Effects of St John’s wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide”British Journal of Pharmacology 153 (7): 1579–86.doi:1038/sj.bjp.0707685PMC 2437900PMID 18204476.
  11. ^Park, J; Kim, KA; Park, PW; Park, CW; Shin, JG (2003). “Effect of rifampin on the pharmacokinetics and pharmacodynamics of gliclazide”. Clinical Pharmacology & Therapeutics 74 (4): 334–40. doi:1016/S0009-9236(03)00221-2PMID 14534520.
  12. ^Schernthaner, G.; Grimaldi, A.; Di Mario, U.; Drzewoski, J.; Kempler, P.; Kvapil, M.; Novials, A.; Rottiers, R. et al. (2004). “GUIDE study: Double-blind comparison of once-daily gliclazide MR and glimepiride in type 2 diabetic patients”. European Journal of Clinical Investigation 34 (8): 535–42. doi:1111/j.1365-2362.2004.01381.xPMID 15305887.