Omacetaxine Mepesuccinate (Synribo)

Number: 0872

Table Of Contents

Applicable CPT / HCPCS / ICD-10 Codes


  1. Criteria for Initial Approval

    Aetna considers omacetaxine mepesuccinate (Synribo) medically necessary for the following indications:

    Chronic myeloid leukemia (CML) 

    For treatment of CML confirmed by detection of the Ph chromosome or BCR::ABL gene by cytogenetic and/or molecular testing when all of the following criteria are met:

    1. Member meets any of the following:

      1. Member has chronic or accelerated phase CML; or
      2. Member has received HSCT for CML; and
    2. Member has experienced resistance or intolerance to two or more tyrosine kinase inhibitors (TKIs) (e.g., bosutinib, dasatinib, imatinib, nilotinib, ponatinib); and
    3. The requested medication is used as a single agent.

    Aetna considers all other indications as experimental and investigational (for additional information, see Experimental and Investigational and Background sections).

  2. Continuation of Therapy

    Aetna considers continuation of omacetaxine mepesuccinate (Synribo) therapy medically necessary for treatment of CML when there is no evidence of unacceptable toxicity or disease progression while on the current regimen and either of the following criteria is met:

    1. Member has CML that has been confirmed by detection of Ph chromosome or BCR::ABL gene by cytogenetic and/ or molecular testing; or
    2. Member has received HSCT for CML.

Dosage and Administration

Omacetaxine mepesuccinate (Synribo) is available as a single-dose vial containing 3.5 mg omacetaxine mepesuccinate as a lyophilized powder for subcutaneous injection.

Chronic Myeloid Leukemia

The recommended dosing is as follows:

Induction dose: 1.25 mg/m2 administered subcutaneously twice daily for 14 consecutive days of a 28‐day cycle. Cycles should be repeated every 28 days until patients achieve a hematologic response.

Maintenance dose: 1.25 mg/m2 administered subcutaneously twice daily for 7 consecutive days of a 28‐day cycle. Treatment should continue as long as individuals are clinically benefiting from therapy.

Source: Teva, 2021

Experimental and Investigational

Aetna considers omacetaxine mepesuccinate experimental and investigational for the treatment of the following indications (not an all-inclusive list) because its effectiveness for indications other than the ones listed above has not been established:

  • Acute myelogenous leukemia (AML)
  • Chronic myelomonocytic leukemia (CMML)
  • Diffuse large B-cell lymphoma (DLBCL)
  • Hepatocellular carcinoma
  • Meningiomas
  • Myelodysplastic syndrome (MDS)
  • Solid tumors including cervical carcinoma and renal cell carcinoma.


CPT Codes / HCPCS Codes / ICD-10 Codes

Code Code Description

Other CPT codes related to the CPB:

96372 Therapeutic, prophylactic, or diagnostic injection (specify substance or drug); subcutaneous or intramuscular
96401 Chemotherapy administration, subcutaneous

HCPCS codes covered if selection criteria are met:

J9262 Injection, omacetaxine mepesuccinate, 0.01 mg

Other HCPCS codes related to the CPB:

Tyrosine kinase inhibitors (bosutinib, dasatinib, nilotinib, ponatinib)- No specific code
S0088 Imatinib, 100 mg

ICD-10 codes covered if selection criteria are met:

C92.10 - C92.22 Chronic myeloid leukemia

ICD-10 codes not covered for indications listed in the CPB:

C11.0 - C11.9 Malignant neoplasm of nasopharynx
C15.3 - C15.9 Malignant neoplasm of esophagus
C16.0 - C16.9 Malignant neoplasm of stomach
C18.0 - C18.9 Malignant neoplasm of colon
C19 - C21.8 Malignant neoplasm of rectosigmoid junction, rectum, anus and anal canal
C22.0 Liver cell carcinoma
C22.1 Intrahepatic bile duct carcinoma
C23 - C24.9 Malignant neoplasm of gall bladder and other and unspecified parts of biliary tract
C25.0 - C25.9 Malignant neoplasm of pancreas
C31.0 - C31.9 Malignant neoplasm of accessory sinuses (paranasal)
C33 - C34.92 Malignant neoplasm trachea, bronchus, and lung
C37 Malignant neoplasm of thymus
C40.00 - C41.9 Malignant neoplasm of bone and articular cartilage
C43.0 - C43.9 Malignant melanoma of skin
C47.0 - C47.9
C49.0 - C49.9
Malignant neoplasm of peripheral nerves, autonomic nervous system, connective and soft tissue
C50.011 - C50.929 Malignant neoplasm of breast
C46.1 Kaposi's sarcoma of soft tissue
C53.0 - C53.9 Malignant neoplasm of cervix uteri
C54.0 - C54.9 Malignant neoplasm of corpus uteri
C57.00 - C57.02 Malignant neoplasm of fallopian tube
C61 Malignant neoplasm of prostate
C64.1 - C66.9
C68.0 - C68.9
Malignant neoplasm of kidney and other and unspecified urinary organs
C70.0 - C70.9 Malignant neoplasm of meninges
C71.0 - C71.9 Malignant neoplasm of brain
C72.0 - C72.9 Malignant neoplasm of spinal cord, cranial nerves and other parts of central nervous system
C73 Malignant neoplasm of thyroid gland
C83.30 - C83.39 Diffuse large B-cell lymphoma
C92.00 - C92.02
C92.40 - C92.A2
Acute myeloid leukemia
C93.10 - C93.12 Chronic myelomonocytic leukemia
D32.0 - D32.9 Benign neoplasm of meninges
D46.0 - D46.9 Myelodysplastic syndromes


U.S. Food and Drug Administration (FDA)-Approved Indications

  • Synribo is indicated for the treatment of adult patients with chronic or accelerated phase chronic myeloid leukemia (CML) with resistance and/or intolerance to two or more tyrosine kinase inhibitors (TKIs).

Compendial Uses

  • Treatment of advanced phase CML for patients with disease progression to accelerated phase
  • Follow-up therapy for CML patients after hematopoietic stem cell transplant (HSCT)

Omacetaxine mepesuccinate is available as Synribo (Teva Pharmaceuticals USA, Inc.) is a cetaxine. The pharmacology of Synribo (omacetaxine mepesuccinate) has not been fully elucidated but includes inhibition of protein synthesis and is independent of direct Bcr‐Abl binding. Synribo (omacetaxine mepesuccinate) binds to the A‐site cleft in the peptidyl‐transferase center of the large ribosomal subunit from a strain of archaeabacteria (Teva, 2019).

Synribo (omacetaxine) was approved by the U.S. Food and Drug Administration (FDA) for the treatment of adult patients with chronic or accelerated phase chronic myeloid leukemia (CML) with resistance and/or intolerance to 2 or more tyrosine kinase inhibitors (TKIs). This labeling states that this indication is based upon response rate.  The labeling notes that there are no trials verifying an improvement in disease-related symptoms or increased survival with omacetaxine.

Quintas-Cardama and Cortes (2008) stated that homoharringtonine (HHT), a natural alkaloid extracted from various Cephalotaxus species, exerts its anti-tumoral and anti-angiogenic activity through an inhibition of protein synthesis and the promotion of apoptosis.  ChemGenex Pharmaceuticals Ltd, in collaboration with Stragen Group, is developing omacetaxine mepesuccinate, a semi-synthetic formulation of HHT, as a potential treatment for CML, myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).  In pre-clinical studies, omacetaxine mepesuccinate induced apoptosis in leukemia cell lines.  Results from phase II clinical trials revealed omacetaxine mepesuccinate to be active in patients with CML that was resistant to TKI therapy, including those patients who carry the BCR-ABL1T315I mutation, which is highly insensitive to the TKIs imatinib, nilotinib and dasatinib; the therapeutic was also generally well-tolerated.  Phase II and III clinical trials have been underway to assess the activity of omacetaxine mepesuccinate, either alone or in combination with TKIs or other cytotoxic drugs, in patients with CML that is resistant to TKI therapy.  Phase I and II clinical trials for omacetaxine mepesuccinate in the treatment of AML and MDS are also ongoing; intravenous, subcutaneous (SC) and oral formulations of the drug are being developed.  The authors concluded that omacetaxine mepesuccinate appears to hold potential for the treatment of CML and, in particular, imatinib-resistant CML; the development of alternative formulations of the therapeutic further expands the potential for success in drug development.

Daver et al (2013) noted that HHT (omacetaxine mepesuccinate) is an alkaloid inhibitor of protein synthesis with activity in myeloid malignancies.  In a phase II clinical trial, these investigators reported the findings of a pilot study of HHT in MDS.  Induction consisted of HHT at 2.5 mg/m(2) via continuous infusion for 7 days.  Maintenance was given every 4 weeks.  A total of 9 patients were enrolled: 5 with refractory anemia with excess blasts, 2 with refractory anemia with excess blasts in transformation, 1 each with refractory anemia and CML, respectively.  Median age was 70 years (55 to 84) and 6 (66 %) were males.  Per International Prognostic Scoring System (IPSS), 2 patients were intermediate-1, 5 intermediate-2 and 2 high-risk.  Median chemotherapy courses were 1 (1 to 3).  One patient (11 %) responded with complete hematological and cytogenetic remission after 1 course.  Eight patients did not respond (4 had stable disease, 2 progressed to acute leukemia and 2 died during induction -- from aspergillus pneumonia and intra-cerebral hemorrhage, respectively).  Grade 3/4 myelosuppression seen in 56 % (5/9).  Serious non-hematological toxicities included 1 case of grade 4 left bundle branch heart block and 1 grade 3 nephrotoxicity.  Median time between courses was 42 days (35 to 72 days).  The authors concluded that HHT might have clinical activity in some patients with MDS.

Nemunaitis et al (2013) stated that omacetaxine mepesuccinate is a first-in-class cephalotaxine demonstrating clinical activity in CML.  A SC formulation demonstrated efficacy and safety in phase I/II trials in patients previously treated with greater than or equal to 1 TKI.  These researchers evaluated pharmacokinetics and safety of SC omacetaxine in patients with advanced cancers.  Omacetaxine 1.25 mg/m(2) SC was administered BID, days 1 to 14 every 28 days for 2 cycles, until disease progression or unacceptable toxicity.  Blood and urine were collected to measure omacetaxine concentrations and inactive metabolites.  Adverse events, including QT interval prolongation, were recorded.  Tumor response was assessed at cycle 2 completion.  Pharmacokinetic parameters were estimated from cycle 1, day 1 data in 21 patients with solid tumors or hematologic malignancies and cycle 1, day 11 data in 10 patients.  Omacetaxine was rapidly absorbed, with mean peak plasma concentrations observed within 1 hour, and widely distributed, as evidenced by an apparent volume of distribution of 126.8 L/m(2).  Plasma concentration versus time data demonstrated bi-exponential decay; mean steady-state terminal half-life was 7 hours.  Concentrations of inactive metabolites 4'-DMHHT and cephalotaxine were approximately 10 % of omacetaxine and undetectable in most patients, respectively.  Urinary excretion of unchanged omacetaxine accounted for less than 15 % of the dose.  Grade 3/4 drug-related adverse events included thrombocytopenia (48 %) and neutropenia (33 %).  Two grade 2 increases in QTc interval (greater than 470 ms) were observed and were not correlated with omacetaxine plasma concentration.  No objective responses were observed.  The authors concluded that omacetaxine is well-absorbed after SC administration.  Therapeutic plasma concentrations were achieved with 1.25 mg/m(2) BID, supporting clinical development of this dose and schedule.

Shim et al (2014) noted that anti-cancer chemotherapy usually involves the administration of several anti-cancer drugs that differ in their action mechanisms.  These researchers examined if the combination of omacetaxine mepesuccinate (OMT) and doxorubicin (DOX) could show synergism, and whether the liposomal co-delivery of these 2 drugs could enhance their anti-tumor effects in cervical carcinoma model.  OMT-loaded liposomes (OL) were prepared by loading the drug in the lipid bilayers.  OL were then electrostatically complexed with DOX, yielding double-loaded liposomes (DOL).  DOX-loaded liposomes (DL) were formulated by electrostatic interaction with negatively charged empty liposomes (EL).  The combination index (CI) values were calculated to evaluate the synergism of the 2 drugs.  In-vitro anti-tumor effects against HeLa cells were measured using CCK-8, calcein staining, and crystal violet staining.  In-vivo anti-tumor effects of various liposomes were tested using HeLa cell-bearing mice.  Combination of DOX and OMT had ratio-dependent synergistic activities, with very strong synergism observed at a molar ratio of 4:1 (DOX:OMT).  The sizes of EL, DL, OL, and DOL did not significantly differ, but the zeta potentials of DL and DOL were slightly higher than those of OL and EL.  In-vitro, DOL showed higher anti-tumor activity than OL, DL or EL in cervical carcinoma HeLa cells.  In-vivo, unlike other liposomes, DOL reduced the tumor growths by 98.6 % and 97.3 % relative to the untreated control on day 15 and 25 after the cessation of treatment, respectively.  The authors concluded that these results suggested that liposomal co-delivery of DOX and OMT could synergistically potentiate anti-tumor effects.

In a meta-analysis, Kantarjian et al (2015) provided an overview on the effectiveness of HHT combination regimens to treat AML. Because most of these studies were performed in China, Chinese published clinical studies were used for the analysis. A search for studies from 2006 to 2013 of regimens containing HHT for AML treatment was performed using published studies and Chinese databases in Mandarin. The complete response (CR) and overall response rate (ORR) were analyzed, and the fixed effects model and random effects model (REM) were calculated. The heterogeneity of the studies was calculated using Q homogeneity statistics. The meta-analysis included 21 studies (n = 1,310, n = 229 pediatric, and n = 216 elderly). Homoharringtonine was given in combination with cytarabine, daunorubicin, idarubicin, aclacinomycin, mitoxantrone, or granulocyte colony-stimulating factor. Heterogeneity was seen in all analyzed pools, but it was most pronounced in retrospective studies. Overall, the REM showed a CR rate of 65.2 %. However, in studies in which HHT-containing regimens were compared to regimens without HHT, the CR rates were 69.1 % in randomized trials and 62.8 % in retrospective studies. Additionally, in studies with exclusively elderly patients, the CR rate was considerably lower than it was for the studies with mixed age populations (47.5 % versus 65.2 %). The authors concluded that higher overall CR rates for HHT-containing regimens in AML treatment in the Chinese studies suggested that HHT could be an active agent in the management of AML. Moreover, they stated that additional clinical trials are needed to evaluate the effectiveness of HHT in the treatment of AML.

Acute Myeloid Leukemia

Lam and colleagues (2016) stated that an in-vitro drug-screening platform on patient samples was developed and validated to design personalized treatment for relapsed/refractory AML.  Unbiased clustering and correlation showed that homoharringtonine (HHT), also known as omacetaxine mepesuccinate, exhibited preferential anti-leukemia effect against AML carrying internal tandem duplication of fms-like tyrosine kinase 3 (FLT3-ITD).  It worked synergistically with FLT3 inhibitors to suppress leukemia growth in-vitro and in xenograft mouse models.  Mechanistically, the effect was mediated by protein synthesis inhibition and reduction of short-lived proteins, including total and phosphorylated forms of FLT3 and its down-stream signaling proteins.  A phase II clinical trial of sorafenib and HHT combination treatment in FLT3-ITD AML patients resulted in CR (true or with insufficient hematological recovery) in 20 of 24 patients (83.3 %), reduction of ITD allelic burden, and median leukemia-free survival and overall survival (OS) of 12 and 33 weeks, respectively.  The regimen has successfully bridged 5 patients to allogeneic hematopoietic stem cell transplantation (allo-HSCT) and was well-tolerated in patients unfit for conventional chemotherapy, including elderly and heavily pre-treated patients.  The authors concluded that the findings of this study validated the principle and clinical relevance of in-vitro drug testing and identified an improved treatment for FLT3-ITD AML.  They stated that these results provided the foundation for phase II/III clinical trials to ascertain the clinical effectiveness of FLT3 inhibitors and HHT in combination.

Chronic Myelomonocytic Leukemia (CMML)

Short and colleagues (2019) stated that the outcome of patients with MDS after failure of hypomethylating agents (HMAs) is poor with a median OS of only 4 to 6 months.  Omacetaxine mepesuccinate (OM) is safe and effective in myeloid malignancies but has not been studied in MDS with HMA failure.  In a phase-II clinical trial, these researchers examined the effectiveness of OM in patients with MDS or chronic myelomonocytic leukemia (CMML) who had previously failed or been intolerant to HMAs.  Patients received OM at a dose of 1.25 mg/m2 subcutaneously every 12 hours for 3 consecutive days on a 4- to 7-week schedule.  The primary end-points were the ORR and OS.  A total of 42 patients were enrolled with a median age of 76 years; the ORR was 33 %.  Patients with diploid cytogenetics were more likely to respond to OM than were those with cytogenetic abnormalities (58 % versus 23 %, respectively; p = 0.03).  Overall, the median OS was 7.5 months and 1-year OS rate was 25 %.  Patients with diploid cytogenetics had superior OS to those with cytogenetic abnormalities (median OS of 14.8 versus 6.8 months, respectively; p = 0.01); 2 patients had ongoing response to OM of 2 years or longer (both MDS with diploid cytogenetics and RUNX1 mutation).  The most common grade greater than or equal to 3 adverse events (AEs) were infections in 11 patients (26 %), febrile neutropenia in 4 (10 %), and hemorrhage in 3 (7 %).  The authors concluded that OM was safe and active in patients with MDS or CMML who experienced HMA failure.  These researchers stated that these findings support the further development of OM in this setting, including combination therapies.

Diffuse Large B‑Cell Lymphoma

Zhang and colleagues (2016) examined if omacetaxine mepesuccinate is beneficial in diffuse large B‑cell lymphoma (DLBCL); 2 DLBCL cell lines [a germinal center B cell‑like subtype (GCB) and an activated B cell‑like subtype (ABC)] were treated with omacetaxine mepesuccinate at various concentrations for different durations.  The present study indicated that omacetaxine mepesuccinate exerted pro-apoptotic effects in the 2 cell types in a dose- and time-dependent manner.  The ABC subtype demonstrated increased sensitivity compared with the GCB subtype.  At 40 ng/ml, omacetaxine mepesuccinate exhibited a marked pro-apoptotic effect on DLBCL cells compared with the other tumor cells investigated.  Furthermore, omacetaxine mepesuccinate induced cell cycle arrest at G0/G1 phase, and promoted cell terminal differentiation of pro-B cells.  These researchers noted that the present study demonstrated that omacetaxine mepesuccinate exerted its anti-tumor effect by reducing telomerase activity.  The authors concluded that the findings of the present study demonstrated that omacetaxine mepesuccinate may induce apoptosis and cell cycle arrest, promote cell differentiation, and reduce telomerase activity in DLBCL cells, thus aiding the development of omacetaxine mepesuccinate-based DLBCL therapeutic strategies.

Hepatocellular Carcinoma

Li et al (2021) stated that hepato-cellular carcinoma (HCC) is the 6th most common and the 4th most deadly cancer worldwide. The development cost of new therapeutics is a major limitation in patient outcomes. More importantly, there is a paucity of pre-clinical HCC models in which to test new small molecules. These researchers implemented potentially novel patient-derived organoid (PDO) and patient-derived xenografts (PDX) strategies for high-throughput drug screening. Omacetaxine, an FDA-approved drug for CML, was found to be a top effective small molecule in HCC PDOs. Next, omacetaxine was tested against a larger cohort of 40 human HCC PDOs. Serial dilution experiments demonstrated that omacetaxine was effective at low (nano-molar) concentrations. Mechanistic studies established that omacetaxine inhibited global protein synthesis, with a disproportionate effect on short half-life proteins. High-throughput expression screening identified molecular targets for omacetaxine, including key oncogenes, such as PLK1. The authors concluded that by means of an innovative strategy, these investigators reported that for the 1st time to their knowledge the effectiveness of omacetaxine in HCC. furthermore, these researchers elucidated key mechanisms of omacetaxine action. Lastly, they provided a proof-of-principle basis for future studies employing drug screening PDOs sequenced with candidate validation in PDX models. They stated that future studies are needed to establish a dosing regimen for HCC, as well as the positioning of omacetaxine in the therapeutic arsenal for HCC.


Jungwirth et al (2023) currently there are no systemic therapeutic options for patients with recurrent or refractory (R/R) meningioma. To identify effective drugs, these researchers carried out a large-scale drug screening using FDA-approved drugs on several meningioma cell lines. The impact of the top 4 compounds was evaluated on cell viability, proliferation, colony formation, migration, and apoptosis. Furthermore, the anti-neoplastic effects of the selected drugs were validated in a heterotopic xenograft mouse model. Analyses of the viability of meningioma cells treated with 119 anti-neoplastic FDA-approved drugs resulted in categorization into sensitive and resistant drug-response groups based on the mean IC50 values and peak serum concentrations (Cmax) in patients. A total of 80 drugs, including 15 alkylating agents, 14 anti-metabolites, and 13 TKIs, were classified as resistant (IC50 greater than Cmax). The sensitive drug-response group (n = 29, IC50 less than Cmax) included RNA/protein synthesis inhibitors, proteasome inhibitors, topoisomerase, tyrosine-kinase, and partial histone deacetylase and microtubule inhibitors. The IC50 value of the 4 most effective compounds (carfilzomib, omacetaxine, ixabepilone, and romidepsin) ranged from 0.12 to 9.5 nmol/L. Most of them caused cell-cycle arrest in the G2-M-phase and induced apoptosis. In addition, all drugs except romidepsin significantly inhibited tumor growth in-vivo. The strongest anti-neoplastic effect was observed for ixabepilone, which reduced tumor volume by 86 %. The authors concluded that a large-scale drug screening provided a comprehensive insight into the anti-meningioma activities of FDA-approved drugs, and identified carfilzomib, omacetaxine, ixabepilone, and romidepsin as novel potent anti-neoplastic agents for the treatment of aggressive meningiomas. The most pronounced effects were observed with ixabepilone mandating for further clinical investigation.

Renal Cell Carcinoma

Wolff et al (2015) noted that renal cell carcinoma (RCC) accounts for 85 % of primary renal neoplasms, and is rarely curable when metastatic. Approximately 70 % of RCCs are clear-cell type (ccRCC), and in greater than 80 % the von Hippel-Lindau (VHL) gene is mutated or silenced. These researchers developed a novel, high-content, screening strategy for the identification of small molecules that are synthetic lethal with genes mutated in cancer. In this strategy, the screen and counter-screen are conducted simultaneously by differentially labeling mutant and reconstituted isogenic tumor cell line pairs with different fluorochromes and using a highly sensitive high-throughput imaging-based platform. This approach minimizes confounding factors from sequential screening, and more accurately replicates the in-vivo cancer setting where cancer cells are adjacent to normal cells. A screen of approximately 12,800 small molecules identified HHT, an FDA-approved drug for treating CML, as a VHL-synthetic lethal agent in ccRCC. Homoharringtonine induced apoptosis in VHL-mutant, but not VHL-reconstituted, ccRCC cells, and inhibited tumor growth in 30 % of VHL-mutant patient-derived ccRCC tumor graft lines tested. Building on a novel screening strategy and utilizing a validated RCC tumorgraft model recapitulating the genetics and drug responsiveness of human RCC, these studies identified HHT as a potential therapeutic agent for a subset of VHL-deficient ccRCCs.


Tyrosine Kinase Inhibitors (TKIs)

  • Gleevec® (imatinib)
  • Tasigna® (nilotinib)
  • Sprycel® (dasatinib)
  • Bosulif® (bosutinib)


The above policy is based on the following references:

  1. Cortes J, Lipton J, Delphine R, et al, Phase 2 study of subcutaneous omacetaxine mepesuccinate after TKI failure in patients with chronic-phase CML with T315I mutation. Blood. 2012;120(13):2573-2580.
  2. Daver N, Vega-Ruiz A, Kantarjian HM, et al. A phase II open-label study of the intravenous administration of homoharringtonine in the treatment of myelodysplastic syndrome. Eur J Cancer Care (Engl). 2013;22(5):605-611.
  3. Jungwirth G, Yu T, Liu F, et al. Pharmacological landscape of FDA-approved anticancer drugs reveals sensitivities to ixabepilone, romidepsin, omacetaxine, and carfilzomib in aggressive meningiomas. Clin Cancer Res. 2023;29(1):233-243.
  4. Kantarjian H, O'Brien S, Jabbour E, et al. Effectiveness of homoharringtonine (omacetaxine mepesuccinate) for treatment of acute myeloid leukemia: A meta-analysis of Chinese studies. Clin Lymphoma Myeloma Leuk. 2015;15(1):13-21
  5. Lam SS, Ho ES, He BL, et al. Homoharringtonine (omacetaxine mepesuccinate) as an adjunct for FLT3-ITD acute myeloid leukemia. Sci Transl Med. 2016;8(359):359ra129.
  6. Li L, Halpert G, Lerner MG, et al. Protein synthesis inhibitor omacetaxine is effective against hepatocellular carcinoma. JCI Insight. 2021;6(12):e138197.
  7. National Comprehensive Cancer Network (NCCN). Omacetaxine. NCCN Drug & Biologics Compendium. Plymouth Meeting, PA: NCCN; April 2023.
  8. National Comprehensive Cancer Network (NCCN). Chronic myeloid leukemia. NCCN Clinical Practice Guidelines in Oncology, Version 2.2023. Plymouth Meeting, PA: NCCN; April 2023.
  9. Nemunaitis J, Mita A, Stephenson J, et al. Pharmacokinetic study of omacetaxine mepesuccinate administered subcutaneously to patients with advanced solid and hematologic tumors. Cancer Chemother Pharmacol. 2013;71(1):35-41.
  10. Quintas-Cardama A, Cortes J. Omacetaxine mepesuccinate -- a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies. IDrugs. 2008;11(5):356-372.
  11. Shim G, Lee S, Choi J, et al. Liposomal co-delivery of omacetaxine mepesuccinate and doxorubicin for synergistic potentiation of antitumor activity. Pharm Res. 2014;31(8):2178-2185.
  12. Short NJ, Jabbour E, Naqvi K, et al. A phase II study of omacetaxine mepesuccinate for patients with higher-risk myelodysplastic syndrome and chronic myelomonocytic leukemia after failure of hypomethylating agents. Am J Hematol. 2019;94(1):74-79.
  13. Teva Pharmaceuticals USA, Inc. Synribo (omacetaxine mepesuccinate) for injection, for subcutaneous use. Prescribing Information. Parsippany, NJ: Teva; revised May 2021.
  14. Wei H, Wang Y, Gale RP, et al. Randomized trial of intermediate-dose cytarabine in induction and consolidation therapy in adults with acute myeloid leukaemia. Clin Cancer Res. 2020;26(13):3154-3161.
  15. Wolff NC, Pavia-Jimenez A, Tcheuyap VT, et al. High-throughput simultaneous screen and counterscreen identifies homoharringtonine as synthetic lethal with von Hippel-Lindau loss in renal cell carcinoma. Oncotarget. 2015;6(19):16951-16962.
  16. Zhang C, Lam SSY, Leung GMK, et al. Sorafenib and omacetaxine mepesuccinate as a safe and effective treatment for acute myeloid leukemia carrying internal tandem duplication of Fms-like tyrosine kinase 3. Cancer. 2020;126(2):344-353.
  17. Zhang L, Chen Z, Zuo W, et al. Omacetaxine mepesuccinate induces apoptosis and cell cycle arrest, promotes cell differentiation, and reduces telomerase activity in diffuse large B‑cell lymphoma cells. Mol Med Rep. 2016;13(4):3092-3100.