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Cardiac arrhythmia is a well-known complication of treatment with IMiDs and chemotherapy. Two of our patients developed grade 3 arrhythmias that necessitated temporary discontinuation of treatment in one and withdrawal from the study in another. It would be prudent therefore to regularly monitor the cardiac status of elderly patients receiving this agent. The major DLT was haematological with http://www.selleckchem.com/products/LY294002.html neutropenia developing in 41% of patients, although grade 3�C4 toxicity was only seen in 19%. Non-haematological grade 3�C4 toxicity occurred in http://www.selleck.cn/products/wortmannin.html study are similar to those seen in MM009 and MM010 studies (Dimopoulos et?al, 2007; Weber et?al, 2007), suggesting that cyclophosphamide does not add significantly to haematological toxicity. The toxicity profile also seems to differ from the combination of melphalan and prednisolone with lenalidomide (MPR), where Grade 3�C4 haematological toxicity at a level of 52��4% was seen at the MTD level (Palumbo et?al, 2007). The difference in myelosuppression with cyclophosphamide compared to melphalan is consistent with the CRD combination being a safer and more tolerable regimen than MPR. The addition of cyclophosphamide in this study increased the overall response rate (CR?+?VGPR?+?PR) to 81%, which is superior to that reported for lenalidomide alone (17�C23%) (Armoiry et?al, 2008) or in combination with dexamethasone (48�C51%) (Wang et?al, 2008). These responses were observed despite a median number of lines of prior therapy of 3 (range 1�C6), used in this study compared to that seen in the MM009 and MM010 trials where up to one-third of patients http://www.selleckchem.com/products/CHIR-99021.html were treated at first relapse. These responses are also higher than our previously reported CR?+?PR response rates of 65% in a retrospective audit of patients receiving a combination of lenalidomide, cyclophosphamide and dexamethasone (Morgan et?al, 2007), all of whom had end-stage disease. Responses after relapse from first-line treatment for myeloma are generally short-lived, with outcomes being determined by the presence of adverse co-morbidities, cytogenetic abnormalities and the adverse side-effects profile of re-induction treatment. In both first and subsequent relapses, increasing drug resistance and accumulated myelo- and nephrotoxicity restrict the intensity of drug that can safely be delivered. Few studies have examined the survival of patients after first relapse.