Decitabine (Dacogen)

Number: 0868


Aetna considers decitabine (Dacogen) medically necessary for members with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).

Aetna considers decitabine experimental and investigational for the following indications (not an all-incluisve list):

  • Chronic myelogenous leukemia (CML)
  • Colon cancer
  • Glioblastoma
  • Head and neck cancers
  • Hepatobiliary cancers (e.g., cholangiocarcinoma and hepato-cellular carcinoma)
  • Lung cancer
  • Melanoma
  • Multiple myeloma
  • Neuroblastoma
  • Ovarian cancer
  • Sarcomas (e.g., Ewing's sarcoma, osteosarcoma and rhabdomyosarcoma)

Dacogen has been approved by the Food and Drug Adminstration (FDA) for myelodysplastic syndromes (MDS): "Decitabine for injection is indicated for treatment of patients with myelodysplastic syndromes (MDS) including previously treated and untreated, de novo and secondary MDS of all French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia) and intermediate-1, intermediate-2, and high-risk International Prognostic Scoring System groups”.

Guidelines from the National Comprehensive Cancer Network indicate Dacogen for the following indications:

  • Myelodysplastic syndromes (MDS) -- Treatment in higher risk patients who

    • Are not candidates for high-intensity therapy
    • Are high-intensity therapy candidates awaiting improved patient status or donor availability
    • Relapse after allogeneic hemopoietic stem cell transplant [2A]
  • Myelodysplastic syndromes -- Treatment in lower risk patients with symptomatic anemia, del(5q) with or without other cytogenetic abnormalities, and serum erythropoietin levels greater than 500 mU/ml with no response or intolerance to lenalidomide and low probability of response to immusuppressive therapy [2A]

  • Myelodysplastic syndromes -- Initial treatment in lower risk patients with

    • Symptomatic anemia and serum erythropoietin levels greater than 500 mU/ml with no del(5q) with or without other cytogenetic abnormalities and a low probability of response to immunosuppressive therapy
    • Clinically relevant thrombocytopenia or neutropenia, or increased marrow blasts [2A]
  • Acute myeloid leukemia (AML) -- Used as a single agent for low-intensity therapy in patients age greater than or equal to 60 years as

    • Induction therapy
    • Post-remission therapy [2A]
  • Acute myeloid leukemia (AML) -- Used as a single agent in patients who cannot tolerate more agressive regimens for

    • Post-induction therapy in patients age less than 60 years with induction failure
    • Salvage chemotherapy [2A]

Kantarjian et al (2003) evaluated the activity and toxicity of decitabine in different phases of chronic myelogenous leukemia (CML).  A total of 130 patients with CML were treated: 123 with Philadelphia chromosome (Ph)-positive CML (64 blastic, 51 accelerated, 8 chronic) and 7 with Ph-negative CML.  Decitabine was given at 100 mg/m(2) over 6 hours every 12 hours x 5 days (1,000 mg/m(2) per course) in the first 13 patients, 75 mg/m(2) in the subsequent 33 patients, and 50 mg/m(2) in the remaining 84 patients.  A total of 552 courses were given to the 130 patients.  Only 4 patients (3 %) died during the first course from myelosuppressive complications (3 patients) or progressive disease (1 patient).  Of 64 patients in the CML blastic phase, 18 patients (28 %) achieved objective responses.  Of these 18 patients, 6 achieved complete hematologic responses (CHR), 2 achieved partial hematologic responses (PHR), 7 achieved hematologic improvements (HI), and 3 returned to the second chronic phase (second CP).  Five patients (8 %) had cytogenetic responses.  Among 51 patients in the accelerated phase, 28 patients (55 %) achieved objective responses (12 CHR, 10 PHR, 3 HI, and 3 second CP).  Seven patients (14 %) had cytogenetic responses.  Among 8 patients treated in the chronic phase, 5 (63 %) had objective responses.  Of 7 patients treated for Ph-negative CML, 4 (57 %) had objective responses.  There was no evidence of a dose-response effect.  The estimated 3-year survival rate was less than 5 % in the blastic phase and 27 % in the accelerated phase.  The only significant toxicity reported was severe myelosuppression, which was delayed, prolonged, and dose-dependent.  With decitabine 50 to 75 mg/m(2), the median time to granulocyte recovery above 0.5 x 10(9)/L was about 4 weeks.  Myelosuppression-associated complications included febrile episodes in 37 % and documented infections in 34 %.  The authors concluded that decitabine appeared to have significant anti-CML activity.  They stated that future studies should evaluate lower-dose, longer-exposure decitabine schedules alone in imatinib-resistant CML, as well as combinations of decitabine and imatinib in different CML phases.

In a phase I study, Fang et al (2010) examined the effects of low-dose decitabine combined with carboplatin in patients with recurrent, platinum-resistant ovarian cancer.  Decitabine was administered intravenously daily for 5 days, before carboplatin (area under the curve, 5) on Day 8 of a 28-day cycle.  By using a standard 3 + 3 dose escalation, decitabine was tested at 2 dose levels: 10 mg/m(2) (7 patients) or 20 mg/m(2) (3 patients).  Peripheral blood mononuclear cells (PBMCs) and plasma collected on Days 1 (pre-treatment), 5, 8, and 15 were used to assess global (LINE-1 repetitive element) and gene-specific DNA methylation.  Dose-limiting toxicity (DLT) at the 20-mg/m(2) dose was grade 4 neutropenia (2 patients), and no DLTs were observed at 10 mg/m(2).  The most common toxicities were nausea, allergic reactions, neutropenia, fatigue, anorexia, vomiting, and abdominal pain, the majority being grades 1 to 2.  One complete response was observed, and 3 additional patients had stable disease for greater than or equal to 6 months.  LINE-1 hypomethylation on Days 8 and 15 was detected in DNA from PBMCs.  Of 5 ovarian cancer-associated methylated genes, HOXA11 and BRCA1 were demethylated in plasma on Days 8 and 15.  The authors concluded that repetitive low-dose decitabine was tolerated when combined with carboplatin in ovarian cancer patients, and demonstrated biological (i.e., DNA-hypomethylating) activity, justifying further testing for clinical efficacy.

In a phase II clinical trial, Glasspool et al (2014) tested the hypothesis that decitabine can reverse resistance to carboplatin in women with relapsed ovarian cancer.  Patients progressing 6 to 12 months after previous platinum therapy were randomized to decitabine on day 1 and carboplatin (AUC 6) on day 8, every 28 days or carboplatin alone.  The primary objective was response rate in patients with methylated hMLH1 tumor DNA in plasma.  After a pre-defined interim analysis, the study closed due to lack of efficacy and poor treatment deliverability in 15 patients treated with the combination.  Responses by GCIG criteria were 9 out of 14 versus 3 out of 15 and by RECIST were 6 out of 13 versus 1 out of 12 for carboplatin and carboplatin/decitabine, respectively.  Grade 3/4 neutropenia was more common with the combination (60 % versus 15.4 %) as was G2/3 carboplatin hypersensitivity (47 % versus 21 %).  The authors concluded that with this schedule, the addition of decitabine appeared to reduce rather than increase the efficacy of carboplatin in partially platinum-sensitive ovarian cancer; and was difficult to deliver.  The authors stated that patient-selection strategies, different schedules and other demethylating agents should be considered in future combination studies.

Xia et al (2014) explored the safety and tolerability of combining 2 epigenetic drugs: decitabine (a DNA methyltransferase inhibitor) and panobinostat (a histone deacetylase inhibitor), with chemotherapy with temozolomide (an alkylating agent).  The purpose of such combination was to evaluate the use of epigenetic priming to overcome resistance of melanoma to chemotherapy.  This phase I clinical trial enrolled patients aged 18 years or older, with recurrent or unresectable stage III or IV melanoma of any site.  Patients were treated with subcutaneous decitabine 0.1 or 0.2 mg/kg 3 times weekly for 2 weeks (starting on day 1), in combination with oral panobinostat 10, 20, or 30 mg every 96 h (starting on day 8), and oral temozolomide 150 mg/m(2)/day on days 9 through 13. In cycle 2, temozolomide was increased to 200 mg/m(2)/day if neutropenia or thrombocytopenia had not occurred.  Each cycle lasted 6 weeks, and patients could receive up to 6 cycles.  Patients who did not demonstrate disease progression were eligible to enter a maintenance protocol with combination of weekly panobinostat and thrice-weekly decitabine until tumor progression, unacceptable toxicity, or withdrawal of consent.  A total of 20 patients were initially enrolled, with 17 receiving treatment.  The median age was 56 years; 11 (65 %) were males, and 6 (35 %) were females.  Eleven (64.7 %) had cutaneous melanoma, 4 (23.5 %) had ocular melanoma, and 2 (11.8 %) had mucosal melanoma.  All patients received at least 1 treatment cycle and were evaluable for toxicity.  Patients received a median of two 6-week treatment cycles (range of 1 to 6).  None of the patients experienced DLT; MTD was not reached.  Adverse events attributed to treatment included grade 3 lymphopenia (24 %), anemia (12 %), neutropenia (12 %), and fatigue (12 %), as well as grade 2 leukopenia (30 %), neutropenia (23 %), nausea (23 %), and lymphopenia (18 %).  The most common reason for study discontinuation was disease progression.  The authors concluded that this triple agent of dual epigenetic therapy in combination with traditional chemotherapy was generally well-tolerated by the cohort and appeared safe to be continued in a phase II trial.  No DLTs were observed, and MTD was not reached.

Lou et al (2014) stated that despite recent advances in the treatment of human colon cancer, the chemotherapy efficacy against colon cancer is still unsatisfactory.  In the present study, effects of concomitant inhibition of the epidermal growth factor receptor (EGFR) and DNA methyltransferase were examined in human colon cancer cells.  These researchers demonstrated that decitabine (a DNA methyltransferase inhibitor) synergized with gefitinib (an EGFR inhibitor) to reduce cell viability and colony formation in SW1116 and LOVO cells.  However, the combination of the 2 compounds displayed minimal toxicity to NCM460 cells, a normal human colon mucosal epithelial cell line.  The combination was also more effective at inhibiting the AKT/mTOR/S6 kinase pathway.  In addition, the combination of decitabine with gefitinib markedly inhibited colon cancer cell migration.  Furthermore, gefitinib synergistically enhanced decitabine-induced cytotoxicity was primarily due to apoptosis as shown by Annexin V labeling that was attenuated by z-VAD-fmk, a pan caspase inhibitor.  Concomitantly, cell apoptosis resulting from the co-treatment of gefitinib and decitabine was accompanied by induction of BAX, cleaved caspase 3 and cleaved PARP, along with reduction of Bcl-2 compared to treatment with either drug alone.  Interestingly, combined treatment with these 2 drugs increased the expression of XIAP-associated factor 1 (XAF1), which play an important role in cell apoptosis.  Moreover, small interfering RNA (siRNA) depletion of XAF1 significantly attenuated colon cancer cells apoptosis induced by the combination of the 2 drugs.  The authors stated that these findings suggested that gefitinib in combination with decitabine exerted enhanced cell apoptosis in colon cancer cells were involved in mitochondrial-mediated pathway and induction of XAF1 expression.  These investigators concluded that based on the observations from this study, they suggested that the combined administration of these 2 drugs might be considered as a novel therapeutic regimen for treating colon cancer.

Maes et al (2014) noted that DNA methyltransferase inhibitors (DNMTi) and histone deacetylase inhibitors (HDACi) are under investigation for the treatment of cancer, including the plasma cell malignancy multiple myeloma (MM). Evidence exists that DNA damage and repair contribute to the cytotoxicity mediated by the DNMTi decitabine. Here, we investigated the DNA damage response (DDR) induced by decitabine in MM using 4 human MM cell lines and the murine 5T33MM model. In addition, we explored how the HDACi JNJ-26481585 affects this DDR. Decitabine induced DNA damage (gamma-H2AX foci formation), followed by a G0/G1- or G2/M-phase arrest and caspase-mediated apoptosis. JNJ-26481585 enhanced the anti-MM effect of decitabine both in vitro and in vivo. As JNJ-26481585 did not enhance decitabine-mediated gamma-H2AX foci formation, we investigated the DNA repair response towards decitabine and/or JNJ-26481585. Decitabine augmented RAD51 foci formation (marker for homologous recombination (HR)) and/or 53BP1 foci formation (marker for non-homologous end joining (NHEJ)). Interestingly, JNJ-26481585 negatively affected basal or decitabine-induced RAD51 foci formation. Finally, B02 (RAD51 inhibitor) enhanced decitabine-mediated apoptosis. Together, we report that decitabine-induced DNA damage stimulates HR and/or NHEJ. JNJ-26481585 negatively affects RAD51 foci formation, thereby providing an additional explanation for the combinatory effect between decitabine and JNJ-26481585.


Everson et al (2015) stated that immunotherapy is an ideal treatment modality to specifically target the diffusely infiltrative tumor cells of malignant gliomas while sparing the normal brain parenchyma. However, progress in the development of these therapies for glioblastoma has been slow due to the lack of immunogenic antigen targets that are expressed uniformly and selectively by gliomas. These researchers utilized human glioblastoma cell cultures to induce expression of New York-esophageal squamous cell carcinoma (NY-ESO-1) following in-vitro treatment with the demethylating agent decitabine. They then investigated the phenotype of lymphocytes specific for NY-ESO-1 using flow cytometry analysis and cytotoxicity against cells treated with decitabine using the xCelligence real-time cytotoxicity assay. Finally, these investigators examined the in-vivo application of this immune therapy using an intra-cranially implanted xenograft model for in-situ T cell trafficking, survival, and tissue studies. These studies showed that treatment of intra-cranial glioma-bearing mice with decitabine reliably and consistently induced the expression of an immunogenic tumor-rejection antigen, NY-ESO-1, specifically in glioma cells and not in normal brain tissue. The up-regulation of NY-ESO-1 by intra-cranial gliomas was associated with the migration of adoptively transferred NY-ESO-1-specific lymphocytes along white matter tracts to these tumors in the brain. Similarly, NY-ESO-1-specific adoptive T cell therapy demonstrated anti-tumor activity after decitabine treatment and conferred a highly significant survival benefit to mice bearing established intracranial human glioma xenografts. Transfer of NY-ESO-1-specific T cells systemically was superior to intra-cranial administration and resulted in significantly extended and long-term survival of animals. The authors concluded that these results revealed an innovative, clinically feasible strategy for the treatment of glioblastoma.

Head and Neck Cancers:

Viet and colleagues (2014) stated that cisplatin resistance in head and neck squamous cell carcinoma (HNSCC) reduces survival. In this study these investigators hypothesized that methylation of key genes mediates cisplatin resistance. They determined whether a demethylating drug, decitabine, could augment the anti-proliferative and apoptotic effects of cisplatin on SCC-25/CP, a cisplatin-resistant tongue SCC cell line. These researchers showed that decitabine treatment restored cisplatin sensitivity in SCC-25/CP and significantly reduced the cisplatin dose required to induce apoptosis. They then created a xenograft model with SCC-25/CP and determined that decitabine and cisplatin combination treatment resulted in significantly reduced tumor growth and mechanical allodynia compared to control. To establish a gene classifier these researchers quantified methylation in cancer tissue of cisplatin-sensitive and cisplatin-resistant HNSCC patients. Cisplatin-sensitive and cisplatin-resistant patient tumors had distinct methylation profiles. When these investigators quantified methylation and expression of genes in the classifier in HNSCC cells in-vitro, they showed that decitabine treatment of cisplatin-resistant HNSCC cells reversed methylation and gene expression toward a cisplatin-sensitive profile. The authors concluded that the findings of this study provided direct evidence that decitabine restored cisplatin sensitivity in in-vitro and in-vivo models of HNSCC. Combination treatment of cisplatin and decitabine significantly reduced HNSCC growth and HNSCC pain. Furthermore, gene methylation could be used as a biomarker of cisplatin-resistance.

National Comprehensive Cancer Network’s clinical practice guideline on “Head and neck cancers” (Version 1.2015) does not list decitabine as a therapeutic option.

Hepatobiliary Cancers:

Wang et al (2014) noted that decitabine (DAC), an inhibitor of DNA methyltransferase, demonstrates anti-tumor activities in various types of cancer. However, its therapeutic potential for cholangiocarcinoma (CCA) remains to be explored. The present study investigated the anti-proliferative effects of DAC on CCA cells in-vitro and in-vivo. Human CCA cell lines, TFK-1 and QBC939, were used as models to investigate DAC on the cell growth and proliferation of CCA. Cell proliferation was evaluated by Cell Counting Kit-8 assay combined with clonogenic survival assay. Flow cytometry, Hoechst 33342/propidium iodide staining and green fluorescent protein-tagged MAP-LC3 detection were applied to determine cell cycle progression, apoptosis and autophagy. Nude mice with TFK-1 xenografts were evaluated for tumor growth following DAC treatment. Decitabine was observed to significantly suppress the proliferation of cultured TFK-1 and QBC939 cells, accompanied with enhanced apoptosis, autophagy and cell cycle arrest at G2/M phase. In TFK-1 mouse xenografts, DAC retarded the tumor growth and increased the survival of CCA tumor-bearing mice.

In an open-label, single-arm, phase I/II study, Mei et al (2015) determined the safety and effectiveness of lower-dose decitabine-based therapy in pre-treated patients with advanced hepato-cellular carcinoma (HCC). The administered dose of decitabine was 6 mg/m2/day intravenously on days 1 to 5 of a 28-day cycle. Additional therapies were given based on their disease progression status. The end-point was to ensure the safety, hepatotoxicity, clinical responses, progression-free survival (PFS) and pharmacodynamics assay of lower-dose decitabine. A total of 15 patients were enrolled. The favorable adverse events and liver function profiles were observed. The most beneficial responses were 1 complete response (CR), 6 stable disease (SD), and 8 progressive disease (PD); MRI liver scans post-treatment indicated a unique and specific characteristic. The immunohistochemistry result from the liver biopsy exhibited noteworthy cytotoxic lymphocytes (CTLs) responses. Median PFS was 4 months (95 % confidence interval [CI]: 1.7 to 7.0), comparing favorably with existing therapeutic options. Expression decrement of DNA methyltransferase DNMT1 and global DNA hypo-methylation were observed in PBMCs after lower-dose decitabine treatment. The authors concluded that the lower-dose decitabine-based treatment resulted in beneficial clinical response and favorable toxicity profiles in patients with advanced HCC. They stated that prospective evaluations of decitabine administration schemes and tumor tissue-based pharmacodynamics effect are needed in future trials.

Furthermore, NCCN’s clinical practice guideline on “Hepatobiliary cancers” (Version 2.2015) does not list decitabine as a therapeutic option

Lung Cancer:

Yan and colleagues (2015) stated that lung cancer cells are sensitive to 5-aza-2'-deoxycytidine (decitabine) or midostaurin (PKC412), because decitabine restores the expression of methylation-silenced tumor suppressor genes, whereas PKC412 inhibits hyperactive kinase signaling, which is essential for cancer cell growth. These researchers demonstrated that resistance to decitabine (decitabine(R)) or PKC412 (PKC412(R)) eventually results from simultaneously re-methylated DNA and re-activated kinase cascades. Indeed, both decitabine(R) and PKC412(R) displayed the up-regulation of DNMT1 and tyrosine-protein kinase (KIT), the enhanced phosphorylation of KIT and its downstream effectors, and the increased global and gene-specific DNA methylation with the down-regulation of tumor suppressor gene epithelial cadherin CDH1. Interestingly, decitabine(R) and PKC412(R) had higher capability of colony formation and wound healing than parental cells in-vitro, which were attributed to the hyperactive DNMT1 or KIT, because inactivation of KIT or DNMT1 reciprocally blocked decitabine(R) or PKC412(R) cell proliferation. Further, DNMT1 knockdown sensitized PKC412(R) cells to PKC412; conversely, KIT depletion synergized with decitabine in eliminating decitabine(R). Importantly, when engrafted into nude mice, decitabine(R) and PKC412(R) had faster proliferation with stronger tumorigenicity that was caused by the re-activated KIT kinase signaling and further CDH1 silencing. The authors concluded that these findings identified functional cross-talk between KIT and DNMT1 in the development of drug resistance, implying the reciprocal targeting of protein kinases and DNA methyltransferases as an essential strategy for durable responses in lung cancer.

Neuroblastoma and Sarcomas:

Krishnadas et al (2013) stated that patients with relapsed stage 4 neuroblastoma have an extremely poor long-term prognosis, making the investigation of new agents of interest.  These investigators reported the outcome of the first patient treated in a phase I study for relapsed neuroblastoma, using the chemotherapy agent decitabine to up-regulate cancer testis antigen expression, followed by a dendritic cell vaccine targeting the cancer testis antigens MAGE-A1, MAGE-A3, and NY-ESO-1.  This patient had persistent tumor in his bone marrow after completion of standard therapy for neuroblastoma, including multi-agent chemotherapy, tumor resection, stem cell transplantation, radiation therapy, and anti-GD2 monoclonal antibodies.  His marrow disease persisted despite chemotherapy, which was given while the vaccine was being produced.  After 3 cycles of decitabine and vaccine, this patient achieved a complete remission (CR) and is now 1 year from his last treatment, with no evidence of tumor in his bone marrow or other sites.  This patient was noted to have an increase in MAGE-A3-specific T cells.  The authors noted that this was the first report combining demethylating chemotherapy to enhance tumor antigen expression followed by a cancer antigen vaccine.  Well-designed studies are needed to ascertain the effectiveness of decitabine in the treatment of neuroblastoma.

Krishnadas et al (2015) noted that antigen-specific immunotherapy was studied in a multi-institutional phase I/II study by combining decitabine (DAC) followed by an autologous dendritic cell (DC)/MAGE-A1, MAGE-A3 and NY-ESO-1 peptide vaccine in children with relapsed/refractory solid tumors. Patients aged 2.5 to 15 years with relapsed neuroblastoma, Ewing's sarcoma, osteosarcoma and rhabdomyosarcoma were eligible to receive DAC followed by DC pulsed with overlapping peptides derived from full-length MAGE-A1, MAGE-A3 and NY-ESO-1. The primary end-points were to assess the feasibility and tolerability of this regimen. Each of 4 cycles consisted of week 1: DAC 10 mg/m(2)/day for 5 days and weeks 2 and 3: DC vaccine once-weekly. A total of 15 patients were enrolled in the study, of which 10 were evaluable. Generation of DC was highly feasible for all enrolled patients. The treatment regimen was generally well-tolerated, with the major toxicity being DAC-related myelosuppression in 5/10 patients; 6 of 9 patients developed a response to MAGE-A1, MAGE-A3 or NY-ESO-1 peptides post-vaccine. Due to limitations in number of cells available for analysis, controls infected with a virus encoding relevant genes have not been performed. Objective responses were documented in 1/10 patients who had a complete response. Of the 2 patients who had no evidence of disease at the time of treatment, 1 remained disease-free 2 years post-therapy, while the other experienced a relapse 10 months post-therapy. The authors concluded that the chemoimmunotherapy approach using DAC/DC-CT vaccine was feasible, well-tolerated and resulted in anti-tumor activity in some patients. Moreover, they stated that future trials to maximize the likelihood of T cell responses post-vaccine are needed.


Table 1. French-American- British (FAB) Classification of MDS


% Blasts in Peripheral Blood

% Blasts in Bone Marrow

Survival in Months

Refractory Anemia (RA)




Refractory Anemia with Ringed Sideroblasts (RARS)




Refractory Anemia with Excess Blasts (RAEB)




Refractory Anemia with Excess Blasts in Transformation (RAEB-t)




Chronic Myelomonocytic Leukemia (CMML)




Source: NCCN, 2013; Dacogen prescribing information.

Table 2: International Prognostic Scoring System (IPSS) for MDS

Score Values

Prognostic Variable






BM Blast (%)














2 or 3




Outcomes According to IPSS 



N = 816


N = 759


Prognosis Score

IPSS Subgroup

Patients (%)

Median Survival (yrs) in absence of therapy

Patients (%)

Median AML transformation (yrs)

























Source: NCCN, 2013, Dacogen prescribing information.  

Table 3:  Supportive Care Measures for Myelodysplastic Syndrome


  • Clinical monitoring
  • Psychosocial support
  • Quality-of-life assessment

Iron Chelation:

  • If greater than 20 to 30 RBC transfusions received
  • If ongoing RBC transfusions are anticipated
  • If serum ferritin greater than 2,500 ng/ml (aiming to decrease serum ferritin to less than 1,000 ng/ml)


  • RBC transfusions for symptomatic anemia
  • Platelet transfusions for thrombocytopenic bleeding
  • Irradiated products suggested for transplant candidates

Hematopoeitic Cytokines:

  • EPO
  • GCSF: platelet count monitored
  • Not recommended for routine use
  • Aminocaproic acid or other antifibrinolytic agents may be considered for bleeding refractory to platelet transfusions or profound cytopenias
Aminocaproic acid or other antifibrinolytic agents may be considered for bleeding refractory to platelet transfusions or profound cytopenias

Antibiotics for bacterial infections

CPT Codes / HCPCS Codes / ICD-10 Codes
Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":
ICD-10 codes will become effective as of October 1, 2015:
Other CPT codes related to the CPB:
96360 - 96368 Intravenous infusion
96374 - 96379 Therapeutic, prophylactic, or diagnostic injection; intravenous push
HCPCS codes covered if selection criteria are met:
J0894 Injection, decitabine, 1 mg
ICD-10 codes covered if selection criteria are met:
C92.00 - C92.02
C92.40 - C92.A2
Acute myeloid leukemia (AML)
C92.20 Atypical chronic myeloid leukemia, BCR/ABL-negative, not having achieved remission
C93.00 - C93.02 Acute monoblastic/monocytic leukemia
C94.00 - C94.22 Acute erythroid and megakaryoblastic leukemia
D46.0 - D46.9 Myelodysplastic syndrome (MDS)
ICD-10 codes not covered for indications listed in the CPB (not all-inclusive):
C18.0 - C18.9 Malignant neoplasm of colon
C43.0 - C43.9 Malignant melanoma of skin
C56.1 - C56.9 Malignant neoplasm of ovary
C90.00 - C90.02 Multiple myeloma
C92.10 Chronic myeloid leukemia, BCR/ABL-positive, not having achieved remission
C92.12 Chronic myeloid leukemia, BCR/ABL-positive, in relapse

The above policy is based on the following references:
    1. National Comprehensive Cancer Network (NCCN). Myelodysplastic Syndromes (MDS). NCCN Clinical Practice Guidelines in Oncology. Version.2.2013. Fort Washington, PA: NCCN; 2013.
    2. Dacogen™ [package insert]. Bloomington, MN: MGI Pharma, Inc.; October 2010.
    3. Dacogen™ Formulary Dossier. Bloomington, MN. MGI Pharma, Inc. September 2006.
    4. National Comprehensive Cancer Network. Decitabine. NCCN Drugs and Biologics Compendium. Fort Washington, PA: NCCN; 2013. 
    5. Dacogen. [DrugDex Compendia]. Available at: Accessed June 2011, March 2013.
    6. Dacogen [Clinical Pharmacology Compendia]. Available at: Accessed March 2013.
    7. Kantarjian HM, O'Brien S, Cortes J, et al. Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Cancer. 2003;98(3):522-528.
    8. Fang F, Balch C, Schilder J, et al. A phase 1 and pharmacodynamic study of decitabine in combination with carboplatin in patients with recurrent, platinum-resistant, epithelial ovarian cancer. Cancer. 2010;116(17):4043-4053.
    9. Krishnadas DK, Shapiro T, Lucas K. Complete remission following decitabine/dendritic cell vaccine for relapsed neuroblastoma. Pediatrics. 2013;131(1):e336-e341.
    10. Glasspool RM, Brown R, Gore M3, et al; Scottish Gynaecological Trials Group. A randomised, phase II trial of the DNA-hypomethylating agent 5-aza-2'-deoxycytidine (decitabine) in combination with carboplatin vs carboplatin alone in patients with recurrent, partially platinum-sensitive ovarian cancer. Br J Cancer. 2014;110(8):1923-1929.
    11. Xia C, Leon-Ferre R, Laux D, et al. Treatment of resistant metastatic melanoma using sequential epigenetic therapy (decitabine and panobinostat) combined with chemotherapy (temozolomide). Cancer Chemother Pharmacol. 2014;74(4):691-697.
    12. Lou YF, Zou ZZ, Chen PJ, et al. Combination of gefitinib and DNA methylation inhibitor decitabine exerts synergistic anti-cancer activity in colon cancer cells. PLoS One. 2014;9(5):e97719.
    13. Maes K, De Smedt E, Lemaire M, et al. The role of DNA damage and repair in decitabine-mediated apoptosis in multiple myeloma. Oncotarget. 2014;5(10):3115-3129.
    14. Viet CT, Dang D, Achdjian S, et al. Decitabine rescues cisplatin resistance in head and neck squamous cell carcinoma. PLoS One. 2014;9(11):e112880
    15. Wang B, Li H, Yang R, et al. Decitabine inhibits the cell growth of cholangiocarcinoma in cultured cell lines and mouse xenografts. Oncol Lett. 2014;8(5):1919-1924
    16. National Comprehensive Cancer Network. Clinical practice guideline: Head and neck cancers. Version 1.2015. NCCN: Fort Washington, PA
    17. Fu X, Zhang Y, Wang X, et al. Low dose decitabine combined with taxol and platinum chemotherapy to treat refractory/recurrent ovarian cancer: An open-label, single-arm, phase I/II study. Curr Protein Pept Sci. 2015;16(4):329-336
    18. Krishnadas DK, Shusterman S, Bai F, et al. A phase I trial combining decitabine/dendritic cell vaccine targeting MAGE-A1, MAGE-A3 and NY-ESO-1 for children with relapsed or therapy-refractory neuroblastoma and sarcoma. Cancer Immunol Immunother. 2015;64(10):1251-1260
    19. Mei Q, Chen M, Lu X, et al. An open-label, single-arm, phase I/II study of lower-dose decitabine based therapy in patients with advanced hepatocellular carcinoma. Oncotarget. 2015;6(18):16698-16711
    20. National Comprehensive Cancer Network. Clinical practice guideline: Hepatobiliary cancers. Version 2.2015. NCCN: Fort Washington, PA
    21. Yan F, Shen N, Pang J, et al. The DNA methyltransferase DNMT1 and tyrosine-protein Kinase KIT cooperatively promote resistance to 5-aza-2'-deoxycytidine (decitabine) and midostaurin (PKC412) in lung cancer cells. J Biol Chem. 2015;290(30):18480-18494
    22. Everson RG, Antonios JP, Lisiero DN, et al. Efficacy of systemic adoptive transfer immunotherapy targeting NY-ESO-1 for glioblastoma. Neuro Oncol. 2015 Sep 1 [Epub ahead of print].

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