RARE DISEASE
Skeletal Ewing sarcoma
Skeletal Ewing sarcoma
Skeletal Ewing sarcoma
Synonyms: Osseous Ewing sarcoma
Synonyms: Osseous Ewing sarcoma
Synonyms: Osseous Ewing sarcoma
Drug discovery
20
drugs
With orphan designations
Overview
Skeletal Ewing sarcoma is a rare, aggressive bone malignancy characterized by chromosomal translocations (e.g., EWSR1-FLI1), primarily affecting children and adolescents. Most common in long bones (femur, pelvis, ribs), it often presents with pain, swelling, and pathological fractures. Treatment involves multimodal chemotherapy, surgery, and/or radiotherapy. Despite advancements, metastatic or recurrent disease carries a poor prognosis (5-year survival <30%). Survivors face significant chronic health burdens, including cardiovascular and musculoskeletal complications [1][4][15].
Burden
Survival: 70% 5-year survival in localized cases vs. <30% for metastatic disease [3][5][15].
Chronic morbidity: 30% hypertension, 14% cardiomyopathy, and musculoskeletal impairments in survivors [4].
Late effects: Radiation-linked second malignancies; neurocognitive deficits linked to chronic condition burden [4][17].
Therapies
Chemotherapy: Neoadjuvant/adjuvant regimens (e.g., vincristine, doxorubicin, cyclophosphamide) to shrink tumors and target micrometastases [1][5][16].
Local control: Surgery (limb-salvage preferred) ± radiation, guided by tumor resectability and functional impact [1][12][17].
Investigational: Targeted therapies (e.g., EWSR1-FLI1 inhibitors) and immunotherapies in clinical trials for refractory/metastatic disease [3][8][19].
Categories: rare bone diseases, rare neoplastic diseases
Research Papers
811 drug discovery papers about Skeletal Ewing sarcoma, with 2 first-in-class and 3 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
811 drug discovery papers about Skeletal Ewing sarcoma, with 2 first-in-class and 3 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
2026-04-03 | Abstract 5426: Anatomic origins of primary skeletal tumors effect metastatic and prognostic behaviors.
Abstract Introduction: This study investigates the histology of nonmetastatic primary skeletal tumors related to their anatomic origin and its influence on 5-year survival outcomes. Methodology: Deidentified patient data were obtained from the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) database. Inclusion criteria included: (1) diagnosis of a primary bone cancer with anatomical location of origin, classified using ICD-O-3 anatomic site codes; (2) documented absence of metastasis to the brain, lung, liver, or bone; (3) cause-specific death and survival duration; and (4) available histology codes. Patients were stratified by primary tumor location and histologic sub-type. Kaplan-Meier survival curves were used to estimate survival, and group differences were assessed with pairwise log-rank tests. A p-value <0.05 was considered statistically significant. Results: The top five most common nonmetastatic skeletal tumors by histology are Chondrosarcoma, Osteosarcoma, Chondroma, Ewing Sarcoma, and Diffuse Large B-Cell Lymphoma (DLBCL). The tumor location distribution and 5-year survival for each histological subclass are outlined in Table 1. Conclusion: The differences in anatomic origin of primary bone tumors when controlled for histologic category influences patient mortality. There are distinct differences in overall survival compared among origin sites, signifying a location-based influence on disease severity and survival. The knowledge of anatomic origin differences of survival of various histologic categories of bone cancer can improve clinical decision making and create more accurate, locational based planning when looking at prognosis and disease progression. Citation Format: Matthew Duazo, Aayush Bhatawadekar, Dillon Pekoff, Maria Plummer, Brian Beatty, . Anatomic origins of primary skeletal tumors effect metastatic and prognostic behaviors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5426.
2026-03-02 | Primary breast Ewing sarcoma in a young adult: diagnostic challenges and neoadjuvant chemotherapy success<b></b>
Extra-skeletal Ewing Sarcoma (EES) is a malignant soft-tissue tumor morphologically indistinguishable from osseous Ewing Sarcoma (ES). The Ewing family includes ES, EES, Askin tumor, and peripheral primitive neuroectodermal tumor. About 85% harbor the t(11;22) (q24;q12) fusion by fluorescence in situ hybridization producing a chimeric protein central to pathogenesis. EES is rare, highly aggressive, and prone to recurrence, typically affecting adolescents and young adults and arising in the trunk or lower limbs; primary breast origin is exceptionally uncommon and carries a poor prognosis relative to other breast malignancies and versus other extra-skeletal ES sites. We report the case of a 37-year-old woman with a rapidly enlarging breast mass. Imaging suggested a cystlike lesion; a core biopsy was non-diagnostic. Wide excision established ES. She received neoadjuvant chemotherapy with complete response, followed by mastectomy. This case and literature review underscore the rarity of primary breast ES and the value of neoadjuvant chemotherapy in management.
2026-02-04 | Characterization of stiffness as a biomarker in osteoarthritis and in bone- and soft tissue cancers
Mechanobiology encompasses all of the mechanical processes that influence the cell and its environment. Thereby, the major actors are the cell´s structural components (i.e. cell membrane, cytoskeleton), the components of the extracellular matrix (ECM), and the interface between both (i.e. mechanosensors, adhesion molecules). It is well established that biomechanics plays a critical role in the homeostasis of living tissue, but the concrete mechanisms by which mechanical cues are assimilated and regulate the balance between health and disease are not yet fully understood. In recent decades, atomic force microscopy (AFM) has emerged as the gold standard to measure the foremost mechanical marker of a tissue/cell, namely the stiffness (measured as the Young´s modulus). This parameter provides important information about the state of a living entity, and can be used to investigate a diseased/degenerative condition. In the present work, AFM was employed to characterize the biomechanical alterations occurring during two major disorders from the orthopedic field: osteoarthritis (OA) and bone/soft-tissue cancers. OA is defined as a degenerative joint condition, characterized by articular cartilage destruction. With progression of the disease the chondrocyte organization pattern is evolving, from single string (SS) in healthy cartilage to double string (DS), small cluster (SC), big cluster (BC) and finally diffuse pattern in the most advanced arthritic state. Cartilage discs of 1mm thickness and 4mm diameter were generated from condyles of patient undergoing total knee arthroplasty and were sorted according to the aforementioned cellular patterns. Subsequently the stiffness of the discs was measured with AFM. A stepwise stiffness decrease was observed with an increasing degeneration level, except for the group of the diffuse pattern, which displayed a large data spread with a relatively high stiffness on average. The discs used for those experiments have the advantage of being of appreciable thickness, they exhibit the native cartilage surface at their upmost side and the cells within the tissue are kept alive. They hence represent a suitable model to further investigate articular cartilage degenerative processes in situ. Bone and soft-tissue sarcomas represent a group of diverse cancer entities from mesenchymal origin, with overall poor prognosis. The stiffness of malignant cells of five different bone and soft-tissue sarcoma cell lines were investigated using AFM and were compared to their respective healthy control cells. Osteosarcoma, Ewing sarcoma, fibrosarcoma and rhabdomyosarcoma cells were significantly less stiff than osteoblasts, 66 Mesenchymal stem cells (MSCs), fibroblasts and skeletal muscle cells (SKMCs) respectively, reflecting a typical feature observed in most of the neoplastic transformation. However, chondrosarcoma cells appeared to be stiffer than chondrocytes and the other malignant cell lines. Further cytoskeleton examination using fluorescence microscopy, ELISA and qPCR revealed that if most of the malignant cells displayed a disorganized internal scaffold and a decreased F-actin content, chondrosarcoma maintained a cytoskeletal structure relatively close to the one of the healthy cells, with the microtubule being the most affected components (increase in the β-tubulin gene expression and protein content). These results define the biomechanical fingerprints of the investigated cancer cell lines and expose the related molecular mechanisms. Overall, the work presented in this thesis contributes to the effort of mechanical characterization of the biological systems respectively addressed in the disclosed studies. Understanding the processes underlying the biomechanical properties of cells and tissue is of upmost importance for the development of novel diagnostic and therapy approaches.
2026-01-10 | Age-Related Clinicopathologic Patterns in Ewing Sarcoma (FET::ETS Family): A Comparative Analysis of Pediatric and Adult Patients.
Background: Ewing sarcoma (ES) is a rare, aggressive small round cell sarcoma (SRCS) that peaks in adolescence. Given its rarity, atypical age or site presentations increase the risk of misclassification. This study examines age-related clinicopathological patterns in molecularly confirmed canonical ES (FET::ETS-fused). Methods: Between 2016 and 2025, 90 tumors diagnosed as ES or Ewing-like SRCSs underwent targeted RNA sequencing and/or EWSR1 break-apart fluorescence in situ hybridization. Patients were stratified into three age groups: 0-18, 19-39, and ≥40 years. Clinical, anatomical, pathological, molecular, and treatment/outcome variables were compared across strata. Results: Canonical ES accounted for 84% (76/90) of SRCSs, dominated by EWSR1::FLI1 (89%). ES comprised 91% of SRCSs in children but declined to 75% in older adults. Tumors arose mainly in bone (63%), with a significant age association (p = 0.016): children and young adults were primarily skeletal (73% and 62%), whereas older adults were predominantly extraskeletal (78%). Renal ES clustered in adults ≥40 years (p = 0.003). Classic histology predominated; atypical patterns were more common in extraskeletal tumors but lacked age specificity. Ewing-like SRCSs (n = 14), with heterogeneous or absent fusions, displayed a broader age distribution-including infants and older adults-and a marked extraskeletal predominance (86%, p = 0.001). Metastatic presentation strongly predicted inferior survival (p = 0.025). Treatment was multimodal, with neoadjuvant chemotherapy more frequent in children (90%, p = 0.029). Conclusions: Age significantly influences anatomic presentation and certain treatment choices in ES, whereas histology and survival remain broadly similar across groups. Age-linked extraskeletal trends reinforce the importance of routine molecular testing, particularly in underreported Middle Eastern populations.
2026-01-03 | RUNX2 Represses the EWS-FLI1-mediated Transcription in Ewing's Sarcoma Cells.
Ewing's sarcoma is an aggressive pediatric malignancy driven by specific chromosomal translocations, predominantly leading to the oncogenic fusion protein EWS-FLI1. Runt-related transcription factors 1 and 2 (RUNX1 and RUNX2), which are key transcription factors involved in osteoblastic differentiation and skeletal morphogenesis, are not expressed in Ewing's sarcoma. Our study aimed to elucidate the relationship between the RUNX genes and EWS-FLI1. We used Ewing's sarcoma cell lines (A673 and NCR-EW2). EWS-FLI1 knockdown was achieved using shRNA, while inducible expression of RUNX1, RUNX2, EWS-FLI1, or EWS-ERG was performed using a Tet-on system. Gene and protein expression levels were quantitatively assessed by qPCR and Western blot analysis, respectively. Cell growth was evaluated using spheroid formation and cell viability assays. Truncated RUNX1 or RUNX2 constructs were employed to identify functional domains, with their intracellular localization confirmed by immunostaining. We observed low expression of RUNX1 and RUNX2 in Ewing's sarcoma cells. Notably, EWS-FLI1 knockdown increased RUNX2 gene expression. Conversely, inducible expressions of either RUNX1 or RUNX2 suppressed the expression of EWS-FLI1 target genes and inhibited cell proliferation and spheroid formation. Additionally, the RUNT domain of RUNX1 and RUNX2 was not essential for their inhibitory effect on EWS-FLI1 target gene expression. Importantly, both EWS-FLI1 and EWS-ERG down-regulated RUNX2 gene expression in hTert-RPE1 cells. EWS-FLI1 suppresses RUNX2 gene expression in Ewing's sarcoma cells, and re-expressing RUNX2 inhibits cell growth. These findings suggest that RUNX2 has a negative impact on the oncogenic process in Ewing's sarcoma.
2026-04-03 | Abstract 5426: Anatomic origins of primary skeletal tumors effect metastatic and prognostic behaviors.
Abstract Introduction: This study investigates the histology of nonmetastatic primary skeletal tumors related to their anatomic origin and its influence on 5-year survival outcomes. Methodology: Deidentified patient data were obtained from the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) database. Inclusion criteria included: (1) diagnosis of a primary bone cancer with anatomical location of origin, classified using ICD-O-3 anatomic site codes; (2) documented absence of metastasis to the brain, lung, liver, or bone; (3) cause-specific death and survival duration; and (4) available histology codes. Patients were stratified by primary tumor location and histologic sub-type. Kaplan-Meier survival curves were used to estimate survival, and group differences were assessed with pairwise log-rank tests. A p-value <0.05 was considered statistically significant. Results: The top five most common nonmetastatic skeletal tumors by histology are Chondrosarcoma, Osteosarcoma, Chondroma, Ewing Sarcoma, and Diffuse Large B-Cell Lymphoma (DLBCL). The tumor location distribution and 5-year survival for each histological subclass are outlined in Table 1. Conclusion: The differences in anatomic origin of primary bone tumors when controlled for histologic category influences patient mortality. There are distinct differences in overall survival compared among origin sites, signifying a location-based influence on disease severity and survival. The knowledge of anatomic origin differences of survival of various histologic categories of bone cancer can improve clinical decision making and create more accurate, locational based planning when looking at prognosis and disease progression. Citation Format: Matthew Duazo, Aayush Bhatawadekar, Dillon Pekoff, Maria Plummer, Brian Beatty, . Anatomic origins of primary skeletal tumors effect metastatic and prognostic behaviors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5426.
2026-03-02 | Primary breast Ewing sarcoma in a young adult: diagnostic challenges and neoadjuvant chemotherapy success<b></b>
Extra-skeletal Ewing Sarcoma (EES) is a malignant soft-tissue tumor morphologically indistinguishable from osseous Ewing Sarcoma (ES). The Ewing family includes ES, EES, Askin tumor, and peripheral primitive neuroectodermal tumor. About 85% harbor the t(11;22) (q24;q12) fusion by fluorescence in situ hybridization producing a chimeric protein central to pathogenesis. EES is rare, highly aggressive, and prone to recurrence, typically affecting adolescents and young adults and arising in the trunk or lower limbs; primary breast origin is exceptionally uncommon and carries a poor prognosis relative to other breast malignancies and versus other extra-skeletal ES sites. We report the case of a 37-year-old woman with a rapidly enlarging breast mass. Imaging suggested a cystlike lesion; a core biopsy was non-diagnostic. Wide excision established ES. She received neoadjuvant chemotherapy with complete response, followed by mastectomy. This case and literature review underscore the rarity of primary breast ES and the value of neoadjuvant chemotherapy in management.
2026-02-04 | Characterization of stiffness as a biomarker in osteoarthritis and in bone- and soft tissue cancers
Mechanobiology encompasses all of the mechanical processes that influence the cell and its environment. Thereby, the major actors are the cell´s structural components (i.e. cell membrane, cytoskeleton), the components of the extracellular matrix (ECM), and the interface between both (i.e. mechanosensors, adhesion molecules). It is well established that biomechanics plays a critical role in the homeostasis of living tissue, but the concrete mechanisms by which mechanical cues are assimilated and regulate the balance between health and disease are not yet fully understood. In recent decades, atomic force microscopy (AFM) has emerged as the gold standard to measure the foremost mechanical marker of a tissue/cell, namely the stiffness (measured as the Young´s modulus). This parameter provides important information about the state of a living entity, and can be used to investigate a diseased/degenerative condition. In the present work, AFM was employed to characterize the biomechanical alterations occurring during two major disorders from the orthopedic field: osteoarthritis (OA) and bone/soft-tissue cancers. OA is defined as a degenerative joint condition, characterized by articular cartilage destruction. With progression of the disease the chondrocyte organization pattern is evolving, from single string (SS) in healthy cartilage to double string (DS), small cluster (SC), big cluster (BC) and finally diffuse pattern in the most advanced arthritic state. Cartilage discs of 1mm thickness and 4mm diameter were generated from condyles of patient undergoing total knee arthroplasty and were sorted according to the aforementioned cellular patterns. Subsequently the stiffness of the discs was measured with AFM. A stepwise stiffness decrease was observed with an increasing degeneration level, except for the group of the diffuse pattern, which displayed a large data spread with a relatively high stiffness on average. The discs used for those experiments have the advantage of being of appreciable thickness, they exhibit the native cartilage surface at their upmost side and the cells within the tissue are kept alive. They hence represent a suitable model to further investigate articular cartilage degenerative processes in situ. Bone and soft-tissue sarcomas represent a group of diverse cancer entities from mesenchymal origin, with overall poor prognosis. The stiffness of malignant cells of five different bone and soft-tissue sarcoma cell lines were investigated using AFM and were compared to their respective healthy control cells. Osteosarcoma, Ewing sarcoma, fibrosarcoma and rhabdomyosarcoma cells were significantly less stiff than osteoblasts, 66 Mesenchymal stem cells (MSCs), fibroblasts and skeletal muscle cells (SKMCs) respectively, reflecting a typical feature observed in most of the neoplastic transformation. However, chondrosarcoma cells appeared to be stiffer than chondrocytes and the other malignant cell lines. Further cytoskeleton examination using fluorescence microscopy, ELISA and qPCR revealed that if most of the malignant cells displayed a disorganized internal scaffold and a decreased F-actin content, chondrosarcoma maintained a cytoskeletal structure relatively close to the one of the healthy cells, with the microtubule being the most affected components (increase in the β-tubulin gene expression and protein content). These results define the biomechanical fingerprints of the investigated cancer cell lines and expose the related molecular mechanisms. Overall, the work presented in this thesis contributes to the effort of mechanical characterization of the biological systems respectively addressed in the disclosed studies. Understanding the processes underlying the biomechanical properties of cells and tissue is of upmost importance for the development of novel diagnostic and therapy approaches.
2026-01-10 | Age-Related Clinicopathologic Patterns in Ewing Sarcoma (FET::ETS Family): A Comparative Analysis of Pediatric and Adult Patients.
Background: Ewing sarcoma (ES) is a rare, aggressive small round cell sarcoma (SRCS) that peaks in adolescence. Given its rarity, atypical age or site presentations increase the risk of misclassification. This study examines age-related clinicopathological patterns in molecularly confirmed canonical ES (FET::ETS-fused). Methods: Between 2016 and 2025, 90 tumors diagnosed as ES or Ewing-like SRCSs underwent targeted RNA sequencing and/or EWSR1 break-apart fluorescence in situ hybridization. Patients were stratified into three age groups: 0-18, 19-39, and ≥40 years. Clinical, anatomical, pathological, molecular, and treatment/outcome variables were compared across strata. Results: Canonical ES accounted for 84% (76/90) of SRCSs, dominated by EWSR1::FLI1 (89%). ES comprised 91% of SRCSs in children but declined to 75% in older adults. Tumors arose mainly in bone (63%), with a significant age association (p = 0.016): children and young adults were primarily skeletal (73% and 62%), whereas older adults were predominantly extraskeletal (78%). Renal ES clustered in adults ≥40 years (p = 0.003). Classic histology predominated; atypical patterns were more common in extraskeletal tumors but lacked age specificity. Ewing-like SRCSs (n = 14), with heterogeneous or absent fusions, displayed a broader age distribution-including infants and older adults-and a marked extraskeletal predominance (86%, p = 0.001). Metastatic presentation strongly predicted inferior survival (p = 0.025). Treatment was multimodal, with neoadjuvant chemotherapy more frequent in children (90%, p = 0.029). Conclusions: Age significantly influences anatomic presentation and certain treatment choices in ES, whereas histology and survival remain broadly similar across groups. Age-linked extraskeletal trends reinforce the importance of routine molecular testing, particularly in underreported Middle Eastern populations.
2026-01-03 | RUNX2 Represses the EWS-FLI1-mediated Transcription in Ewing's Sarcoma Cells.
Ewing's sarcoma is an aggressive pediatric malignancy driven by specific chromosomal translocations, predominantly leading to the oncogenic fusion protein EWS-FLI1. Runt-related transcription factors 1 and 2 (RUNX1 and RUNX2), which are key transcription factors involved in osteoblastic differentiation and skeletal morphogenesis, are not expressed in Ewing's sarcoma. Our study aimed to elucidate the relationship between the RUNX genes and EWS-FLI1. We used Ewing's sarcoma cell lines (A673 and NCR-EW2). EWS-FLI1 knockdown was achieved using shRNA, while inducible expression of RUNX1, RUNX2, EWS-FLI1, or EWS-ERG was performed using a Tet-on system. Gene and protein expression levels were quantitatively assessed by qPCR and Western blot analysis, respectively. Cell growth was evaluated using spheroid formation and cell viability assays. Truncated RUNX1 or RUNX2 constructs were employed to identify functional domains, with their intracellular localization confirmed by immunostaining. We observed low expression of RUNX1 and RUNX2 in Ewing's sarcoma cells. Notably, EWS-FLI1 knockdown increased RUNX2 gene expression. Conversely, inducible expressions of either RUNX1 or RUNX2 suppressed the expression of EWS-FLI1 target genes and inhibited cell proliferation and spheroid formation. Additionally, the RUNT domain of RUNX1 and RUNX2 was not essential for their inhibitory effect on EWS-FLI1 target gene expression. Importantly, both EWS-FLI1 and EWS-ERG down-regulated RUNX2 gene expression in hTert-RPE1 cells. EWS-FLI1 suppresses RUNX2 gene expression in Ewing's sarcoma cells, and re-expressing RUNX2 inhibits cell growth. These findings suggest that RUNX2 has a negative impact on the oncogenic process in Ewing's sarcoma.
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Drug Discovery Landscape
20 orphan drug designations for Skeletal Ewing sarcoma.
20 orphan drug designations for Skeletal Ewing sarcoma.
Drug | Therapy type | Regulator | Orphan designation | Approval | Sponsor |
|---|---|---|---|---|---|
Dinutuximab beta | antibodies | EMA | 2026-06-19 | — | Recordati Netherlands B.V. |
dinutuximab beta | antibodies | FDA | 2025-04-25 | — | Recordati Rare Diseases Inc. |
small molecule RBM39-degrader | small molecules | FDA | 2024-10-22 | — | SEED Therapeutics Inc. |
modified messenger RNA encoding USP6 | RNAs | FDA | 2024-09-26 | — | Merlin Biotech Inc. |
padnarsertib | small molecules | FDA | 2024-07-09 | — | Karyopharm Therapeutics Inc. |
2-(2-chlorophenyl)-5-hydroxy-8-((3S,4R)-3-hydroxy-1-methylpiperidin-4-yl)-4-oxo-4H-chromen-7-yl dihydrogen phosphate | small molecules | FDA | 2023-03-14 | — | Sumitomo Pharma America, Inc. |
Cu-64 anti CD99 | antibodies | FDA | 2021-01-05 | — | Advanced Imaging Projects, LLC |
a novel humanized bispecific XmAb T cell recruiting antibody cross-reactive to human and nonhuman primate STEAP1 and CD3 | antibodies | FDA | 2020-07-07 | — | Amgen, Inc. |
18-(p-[131I]-iodophenyl)octadecyl phosphocholine | small molecules | FDA | 2018-07-03 | — | Cellectar Biosciences, Inc. |
ganitumab | antibodies | FDA | 2017-03-21 | — | NantCell, Inc., a wholly-owned subsidiary of ImmunityBio, Inc. |
(E)-N¿-(1-(5-Chloro-2-hydroxy phenyl)Ethylidene)-3-((4-Methyl Piperazin-1-yl) Sulfonyl) Benzohydrazide Mesylate | small molecules | FDA | 2017-01-12 | — | Salarius Pharmaceuticals |
Small molecule Ewing Sarcoma breakpoint region 1/Friend leukemia virus integration 1 fusion protein inhibitor | small molecules | FDA | 2016-06-30 | — | Georgetown University |
ANA-conjugated dactunomycin nanoemulsion | small molecules | FDA | 2015-07-07 | — | NanoSmart Pharmaceuticals, Inc. |
antinuclear antibody conjugated liposomal doxorubicin | antibodies | FDA | 2015-02-03 | — | NanoSmart Pharmaceuticals, Inc. |
bi-shRNA furin and GMCSF Autologous Tumor Cell Vaccine | RNAs | FDA | 2014-10-22 | — | Gradalis, Inc. |
Efdispo | small molecules | FDA | 2013-01-15 | — | TDP Biotherapeutics, Inc. |
phosphorothioate antisense olignucleotide against EWS-Fli-1 | oligonucleotides | FDA | 2008-09-22 | — | The Cure Our Children Foundation |
Full Phosphorothioate Antisense Oligonucleotide against EWS-Fli-1 nanoparticles | oligonucleotides | FDA | 2008-09-22 | — | The Cure Our Children Foundation |
fenretinide | small molecules | FDA | 2007-02-01 | — | Cancer Research UK |
Liposomal N-Acetylglucosminyl-N-Acetylmuramly-L-Ala-D-isoGln-L-Ala -gylcerolidpalmitoyl | other | FDA | 1998-06-10 | — | Endorex Corp. |
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