The statins differ with respect to their ring structure and substituents. These differences in structure affect the pharmacological properties of the statins, such as:
*Affinity for the active site of the HMGR
*Rates of entry into hepatic and non-hepatic tissues
*Availability in the systemic circulation for uptake into non-hepatic tissues
*Routes and modes of metabolic transformation and elimination
Statins have sometimes been grouped into two groups of statins according to their structure.
Type 1 statins
Statins that have substituted decalin-ring structure that resemble the first statin ever discovered, mevastatin have often been classified as type 1 statins due to their structural relationship. Statins that belong to this group are:
*Lovastatin (Figure 2)
*Pravastatin
*Simvastatin
Type 2 statins 
Statins that are fully synthetic and have larger groups linked to the HMG-like moiety are often referred to as type 2 statins. One of the main differences between the type 1 and type 2 statins is the replacement of the butyryl group of type 1 statins by the fluorophenyl group of type 2 statins. This group is responsible for additional polar interactions that causes tighter binding to the HMGR enzyme. Statins that belong to this group are:
*Fluvastatin (Figure 3)
*Cerivastatin
*Atorvastatin
*Rosuvastatin
Lovastatin is derived from a fungus source and simvastatin and pravastatin are chemical modifications of lovastatin and as a result do not differ much in structure from lovastatin. All three are partially reduced napthylene ring structures. Simvastatin and lovastatin are inactive lactones which must be metabolized to their active hydroxy-acid forms in order to inhibit HMGR. Type 2 statins all exist in their active hydroxy-acid forms. Fluvastatin has indole ring structure, while atorvastatin and rosuvastatin have pyrrole and pyrimidine based ring structure respectively. The lipophilic cerivastatin has a pyridine-based ring structure.