treatment for moderate Type II diabetes
- drugs that stimulate insulin secretion= sulfonylureas
- drugs that improve insulin sensitivity= thiazolidinediones
mechanism of action of sulfonylureas
they increase insulin secretion by activating certain membrane channels;
these are the same channels which are activated when glucokinase acts as a sensor of glucose and leads to ATP production, the ATP activating these channels
metformin
-first line of treatment for type 2 diabetes
-supressess liver gluconeogenesis
(as, normally insulin lowers PEPCK activity in cells but in diabetes when this inhibition is lifted gluconeogenesis can increase and contribute to hyperglycemia further)
Diphtheria toxin
- protein synthesis inhibitor
- catalyses covalent modification of eEF2
- inhibits the eEF2 function of translocation in translation in eukaryotes
- leads to death
- one of the deadliest substances known
Ricin
- (protein synthesis inhibitor)
- targets eukaryotes
- depurinates a single adenosine from 28SrRNA
- this inactivates the ribosome and the elongation factors can no longer bind
- it acts catalytically–therefore, one ricin molecule can inactivate 50,000 ribosomes
streptomycin
- antibiotic
- binds to 30S ribosomal subunit
- inhibits initiation at high concentrations
- at lower concentrations, causes misreading of mRNA- resulting mutations slow the rate of bacterial growth
- it was the first really effective drug against tuberculosis
Tetracycline
- inhibits binding of aminoacyl-tRNA to the 30S subunit
- it is a broad-spectrum antibiotic, also effective against rickettsial organisms,mycoplasmas and certain protozoa
Oxazolidines
(e. g. linezolid)
- synthetic antibiotics that are highly resistant against gram-positive bacteria
- they inhibit the formation of the initiation Met tRNA-30S subunit-mRNA complex
Chloramphenicol
- antibiotic
- inhibits peptidyl transferase activity of the 50S subunit
- relatively toxic to humans as it affects mitochondrial protein synthesis
- not used as a general anti-bacterial agent; it is used to target typhoid fever and bacterial meningitis
Erythromycin
-binds to 50S subunit at the entrance to the peptide exit tunnel and blocks the progression of the nascent peptide
(“molecular constipation”)
Actinomycin D
- blocks all RNA synthesis immediately
- binds tightly to dsDNA (by intercalating between neighbouring GC base pairs)
- too toxic for clinical use generally
- its inhibition of growth of rapidly dividing cells makes it an effective therapeutic agent in the treatment of some cancers
Rifamycin (rifampicin)
- an antibiotic
- blocks all bacterial RNA synthesis by binding the b-subunit of RNA polymerase
- doesn’t affect eukaryotic transcription significantly
- used in treatment of tuberculosis
Camptothecin
topoisomerase I inhibitor drug as anti-cancer
etoposide, doxorubicin
Topoisomerase II inhibitors as anti-cancer
Ciprofloxacin
Topoisomerase I inhibitor as anti-biotic
