This means that the dose of carboplatin must be adjusted for any impairment in kidney function.Calvert formula: 
  
    
      
        
          D
          o
          s
          e
        
        (
        
          m
          g
        
        )
        =
        
          A
          U
          C
        
        ⋅
        (
        
          G
          F
          R
        
        +
        25
        )
      
    
    {\displaystyle \mathrm {Dose} (\mathrm {mg} )=\mathrm {AUC} \cdot (\mathrm {GFR} +25)}
  
The typical area under the curve (AUC) for carboplatin ranges from 3-7 (mg/ml)*min.
The nadir of this myelosuppression usually occurs 21–28 days after the first treatment, after which the blood cell and platelet levels in the blood begin to stabilize, often coming close to its pre-carboplatin levels. This decrease in white blood cells (neutropenia) can cause complications, and is sometimes treated with drugs like filgrastim. The most notable complication of neutropenia is increased probability of infection by opportunistic organisms, which necessitates hospital readmission and treatment with antibiotics. Chemistry
In terms of its structure, carboplatin differs from cisplatin in that it has a bidentate dicarboxylate (the ligand is CycloButane DiCarboxylic Acid, CBDCA) in place of the two chloride ligands, which are the leaving groups in cisplatin. For this reason, "CBDCA" is sometimes used in the medical literature as an abbreviation referring to carboplatin. Carboplatin exhibits lower reactivity and slower DNA binding kinetics, although it forms the same reaction products in vitro at equivalent doses with cisplatin. Unlike cisplatin, carboplatin may be susceptible to alternative mechanisms. Some results show that cisplatin and carboplatin cause different morphological changes in MCF-7 cell lines while exerting their cytotoxic behaviour. The diminished reactivity limits protein-carboplatin complexes, which are excreted. The lower excretion rate of carboplatin means that more is retained in the body, and hence its effects are longer lasting (a retention half-life of 30 hours for carboplatin, compared to 1.5-3.6 hours in the case of cisplatin). Mechanism of action
Two theories exist to explain the molecular mechanism of action of carboplatin with DNA:

Aquation, or the like-cisplatin hypothesis.