id stringlengths 22 34 | text stringlengths 29 802 | entities listlengths 2 2 | relations listlengths 1 1 |
|---|---|---|---|
chemprot_train_0_6_2_3 | Recent studies have provided consistent evidence that treatment with abatacept results in a rapid onset of efficacy that is maintained over the course of treatment in patients with inadequate response to @CHEMICAL$ and anti-@GENE-N$ therapies. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
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chemprot_train_1_8_30_9 | @GENE-Y$ inhibitors currently under investigation include the small molecules @CHEMICAL$ (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
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] |
chemprot_train_1_8_30_10 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (@CHEMICAL$, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
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] | [
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"head": 0,
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chemprot_train_1_8_30_11 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, @CHEMICAL$) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
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chemprot_train_1_8_30_12 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and @CHEMICAL$ (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
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"head": 0,
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chemprot_train_1_8_30_13 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (@CHEMICAL$, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
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{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
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"head": 0,
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chemprot_train_1_8_30_14 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, @CHEMICAL$), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
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"role": "head"
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{
"text": "@CHEMICAL$",
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"role": "tail"
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] | [
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chemprot_train_1_8_30_15 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as @CHEMICAL$ (IMC-225, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
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{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
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"head": 0,
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chemprot_train_1_8_30_16 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (@CHEMICAL$, Erbitux). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
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chemprot_train_1_8_30_17 | @GENE-Y$ inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, @CHEMICAL$). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
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{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
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"head": 0,
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chemprot_train_1_9_18_31 | Agents that have only begun to undergo clinical evaluation include @CHEMICAL$, an irreversible pan-@GENE-Y$ tyrosine kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
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chemprot_train_1_9_18_32 | Agents that have only begun to undergo clinical evaluation include @CHEMICAL$, an irreversible pan-erbB @GENE-N$ inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
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"role": "head"
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{
"text": "@GENE-N$",
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"role": "tail"
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] | [
{
"head": 0,
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chemprot_train_1_9_18_33 | Agents that have only begun to undergo clinical evaluation include @CHEMICAL$, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and GW572016, both examples of dual @GENE-N$ inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
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"role": "head"
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{
"text": "@GENE-N$",
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chemprot_train_1_9_18_34 | Agents that have only begun to undergo clinical evaluation include @CHEMICAL$, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting @GENE-Y$ and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
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{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
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"label": "false"
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] |
chemprot_train_1_9_18_35 | Agents that have only begun to undergo clinical evaluation include @CHEMICAL$, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and @GENE-Y$). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
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"label": "false"
}
] |
chemprot_train_1_9_31_19 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-@GENE-Y$ @CHEMICAL$ kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
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"role": "tail"
}
] | [
{
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chemprot_train_1_9_32_19 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @CHEM-GENE$ inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
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] |
chemprot_train_1_9_19_33 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @CHEMICAL$ kinase inhibitor, and PKI166 and GW572016, both examples of dual @GENE-N$ inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
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{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
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"label": "false"
}
] |
chemprot_train_1_9_19_34 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @CHEMICAL$ kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting @GENE-Y$ and Her2). | [
{
"text": "@CHEMICAL$",
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"role": "head"
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{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
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"label": "false"
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] |
chemprot_train_1_9_19_35 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @CHEMICAL$ kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and @GENE-Y$). | [
{
"text": "@CHEMICAL$",
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"role": "head"
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{
"text": "@GENE-Y$",
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"role": "tail"
}
] | [
{
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] |
chemprot_train_1_9_31_20 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-@GENE-Y$ tyrosine kinase inhibitor, and @CHEMICAL$ and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
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{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
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] |
chemprot_train_1_9_32_20 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @GENE-N$ inhibitor, and @CHEMICAL$ and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
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{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
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] |
chemprot_train_1_9_20_33 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and @CHEMICAL$ and GW572016, both examples of dual @GENE-N$ inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_1_9_20_34 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and @CHEMICAL$ and GW572016, both examples of dual kinase inhibitors (inhibiting @GENE-Y$ and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_1_9_20_35 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and @CHEMICAL$ and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and @GENE-Y$). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_1_9_31_21 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-@GENE-Y$ tyrosine kinase inhibitor, and PKI166 and @CHEMICAL$, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_1_9_32_21 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB @GENE-N$ inhibitor, and PKI166 and @CHEMICAL$, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_1_9_21_33 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and @CHEMICAL$, both examples of dual @GENE-N$ inhibitors (inhibiting epidermal growth factor receptor and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_1_9_21_34 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and @CHEMICAL$, both examples of dual kinase inhibitors (inhibiting @GENE-Y$ and Her2). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_1_9_21_35 | Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and @CHEMICAL$, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and @GENE-Y$). | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_2_0_57_68 | Effects of chronic social defeat stress on behavior and @CHEMICAL$ acetyltransferase, 78-kDa glucose-regulated protein, and @GENE-Y$ in adult mice. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_2_0_69_57 | Effects of chronic social defeat stress on behavior and @CHEM-GENE$, 78-kDa glucose-regulated protein, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_2_0_57_70 | Effects of chronic social defeat stress on behavior and @CHEMICAL$ acetyltransferase, @GENE-Y$, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_2_0_58_68 | Effects of chronic social defeat stress on behavior and choline acetyltransferase, 78-kDa @CHEMICAL$-regulated protein, and @GENE-Y$ in adult mice. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_2_0_69_58 | Effects of chronic social defeat stress on behavior and @GENE-Y$, 78-kDa @CHEMICAL$-regulated protein, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_2_0_70_58 | Effects of chronic social defeat stress on behavior and choline acetyltransferase, @CHEM-GENE$, and CCAAT/enhancer-binding protein (C/EBP) homologous protein in adult mice. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_1_76_75 | @GENE-Y$, a recently identified cell surface protease, is the key enzyme of @CHEMICAL$ homoeostasis modulating the expression of the liver peptide hormone hepcidin. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_1_75_80 | Matriptase-2, a recently identified cell surface protease, is the key enzyme of @CHEMICAL$ homoeostasis modulating the expression of the liver peptide hormone @GENE-Y$. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
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"label": "false"
}
] |
chemprot_train_3_1_90_75 | Matriptase-2, a recently identified cell surface @GENE-N$, is the key enzyme of @CHEMICAL$ homoeostasis modulating the expression of the liver peptide hormone hepcidin. | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_77_73 | Taken together, the results of the present study have characterized @GENE-Y$ as an inhibitor of matriptase-2 that modulates the synthesis of hepcidin and provides new insights into the regulatory mechanism of @CHEMICAL$ homoeostasis, with clinical importance for a treatment of iron overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_78_73 | Taken together, the results of the present study have characterized HAI-2 as an inhibitor of @GENE-Y$ that modulates the synthesis of hepcidin and provides new insights into the regulatory mechanism of @CHEMICAL$ homoeostasis, with clinical importance for a treatment of iron overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_79_73 | Taken together, the results of the present study have characterized HAI-2 as an inhibitor of matriptase-2 that modulates the synthesis of @GENE-Y$ and provides new insights into the regulatory mechanism of @CHEMICAL$ homoeostasis, with clinical importance for a treatment of iron overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_77_74 | Taken together, the results of the present study have characterized @GENE-Y$ as an inhibitor of matriptase-2 that modulates the synthesis of hepcidin and provides new insights into the regulatory mechanism of iron homoeostasis, with clinical importance for a treatment of @CHEMICAL$ overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_78_74 | Taken together, the results of the present study have characterized HAI-2 as an inhibitor of @GENE-Y$ that modulates the synthesis of hepcidin and provides new insights into the regulatory mechanism of iron homoeostasis, with clinical importance for a treatment of @CHEMICAL$ overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_3_8_79_74 | Taken together, the results of the present study have characterized HAI-2 as an inhibitor of matriptase-2 that modulates the synthesis of @GENE-Y$ and provides new insights into the regulatory mechanism of iron homoeostasis, with clinical importance for a treatment of @CHEMICAL$ overload diseases. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_4_0_121_126 | @CHEMICAL$ and bromoacetylalprenololmenthane are competitive slowly reversible antagonists at the @GENE-Y$ of rat left atria. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_4_0_122_126 | Alprenolol and @CHEMICAL$ are competitive slowly reversible antagonists at the @GENE-Y$ of rat left atria. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_4_2_108_123 | Alprenolol and @CHEMICAL$ at 10(-7), 3 x 10(-7), and 10(-6) M inhibited the cardiac stimulation response slightly, which is indicative of membrane-stabilizing activity independent of @GENE-N$ blockade. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_4_2_120_123 | @CHEMICAL$ and BAAM at 10(-7), 3 x 10(-7), and 10(-6) M inhibited the cardiac stimulation response slightly, which is indicative of membrane-stabilizing activity independent of @GENE-N$ blockade. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_4_4_110_124 | @CHEMICAL$ and BAAM also caused surmountable antagonism of isoprenaline responses, and this @GENE-Y$ antagonism was slowly reversible. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_4_4_111_124 | Alprenolol and @CHEMICAL$ also caused surmountable antagonism of isoprenaline responses, and this @GENE-Y$ antagonism was slowly reversible. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_4_4_113_124 | Alprenolol and BAAM also caused surmountable antagonism of @CHEMICAL$ responses, and this @GENE-Y$ antagonism was slowly reversible. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:5"
}
] |
chemprot_train_4_6_117_125 | We conclude that @CHEMICAL$ and BAAM are competitive slowly reversible @GENE-Y$ antagonists on rat left atria. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_4_6_118_125 | We conclude that alprenolol and @CHEMICAL$ are competitive slowly reversible @GENE-Y$ antagonists on rat left atria. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:6"
}
] |
chemprot_train_5_6_147_140 | @GENE-Y$ was chemically bound via linkers to @CHEMICAL$-loaded HSA-NP. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_5_6_140_148 | Apolipoprotein E was chemically bound via linkers to @CHEMICAL$-loaded @GENE-Y$-NP. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_0_160_169 | Discovery and optimization of @CHEMICAL$ as inhibitors of methionine aminopeptidase-2: a structural basis for the reduction of @GENE-Y$ binding. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_6_0_160_170 | Discovery and optimization of @CHEMICAL$ as inhibitors of @GENE-Y$: a structural basis for the reduction of albumin binding. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_0_161_169 | Discovery and optimization of anthranilic acid sulfonamides as inhibitors of @CHEMICAL$ aminopeptidase-2: a structural basis for the reduction of @GENE-Y$ binding. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_0_170_161 | Discovery and optimization of anthranilic acid sulfonamides as inhibitors of @CHEM-GENE$: a structural basis for the reduction of albumin binding. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_1_162_157 | @CHEM-GENE$ (MetAP2) is a novel target for cancer therapy. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_1_157_165 | @CHEMICAL$ aminopeptidase-2 (@GENE-Y$) is a novel target for cancer therapy. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_2_163_158 | As part of an effort to discover orally active reversible inhibitors of @GENE-Y$, a series of @CHEMICAL$ with micromolar affinities for human MetAP2 were identified using affinity selection by mass spectrometry (ASMS) screening. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_2_158_164 | As part of an effort to discover orally active reversible inhibitors of MetAP2, a series of @CHEMICAL$ with micromolar affinities for @GENE-Y$ were identified using affinity selection by mass spectrometry (ASMS) screening. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_4_167_159 | Modifications based on structural information on the binding of lead compounds to both @GENE-Y$ and domain III of albumin allowed the identification of compounds with significant improvements in both parameters, which showed good cellular activity in both proliferation and @CHEMICAL$ processing assays. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_6_4_168_159 | Modifications based on structural information on the binding of lead compounds to both MetAP2 and @GENE-N$ allowed the identification of compounds with significant improvements in both parameters, which showed good cellular activity in both proliferation and @CHEMICAL$ processing assays. | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_7_8_189_177 | @GENE-Y$ stimulated @CHEMICAL$ incorporation in these end buds in the absence and presence of epidermal growth factor. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_7_8_177_190 | KGF stimulated @CHEMICAL$ incorporation in these end buds in the absence and presence of @GENE-Y$. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_0_212_207 | Configuration of a scintillation proximity assay for the activity assessment of recombinant @CHEM-GENE$. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_1_208_197 | @CHEM-GENE$ plays a role in purine salvage by catalyzing the direct conversion of adenine to adenosine monophosphate. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_1_208_198 | @GENE-Y$ plays a role in purine salvage by catalyzing the direct conversion of @CHEMICAL$ to adenosine monophosphate. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:9"
}
] |
chemprot_train_8_1_208_199 | @GENE-Y$ plays a role in purine salvage by catalyzing the direct conversion of adenine to @CHEMICAL$. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:9"
}
] |
chemprot_train_8_1_208_205 | @GENE-Y$ plays a role in @CHEMICAL$ salvage by catalyzing the direct conversion of adenine to adenosine monophosphate. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_2_200_209 | The involvement of the @CHEMICAL$ salvage pathway in tumor proliferation and angiogenesis makes @GENE-Y$ a potential target for oncology drug discovery. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_2_209_201 | The involvement of the purine salvage pathway in tumor proliferation and angiogenesis makes @CHEM-GENE$ a potential target for oncology drug discovery. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_3_202_210 | We have expressed and characterized recombinant, @CHEMICAL$-terminally His-tagged @GENE-Y$. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_3_203_210 | We have expressed and characterized recombinant, N-terminally @CHEMICAL$-tagged @GENE-Y$. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_3_210_204 | We have expressed and characterized recombinant, N-terminally His-tagged @CHEM-GENE$. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_8_6_211_206 | We describe here the biochemical characterization of @CHEM-GENE$ and the development of a robust, homogeneous, 384-well assay suitable for high throughput screening. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_9_1_256_228 | BACKGROUND: Since the introduction of the first @GENE-Y$ inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, @CHEMICAL$, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different ph... | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_228_257 | BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, @CHEMICAL$, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly differ... | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_256_229 | BACKGROUND: Since the introduction of the first @GENE-Y$ inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, @CHEMICAL$ and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different phar... | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_229_257 | BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, @CHEMICAL$ and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly differen... | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_256_232 | BACKGROUND: Since the introduction of the first @GENE-Y$ inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and @CHEMICAL$, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharm... | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_232_257 | BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and @CHEMICAL$, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different... | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:4"
}
] |
chemprot_train_9_1_256_242 | BACKGROUND: Since the introduction of the first @GENE-Y$ inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pha... | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_9_1_242_257 | BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly differe... | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "CPR:9"
}
] |
chemprot_train_10_0_337_305 | The effects of mitiglinide (KAD-1229), a new anti-diabetic drug, on @GENE-N$ and insulin secretion: comparison with the @CHEMICAL$ and nateglinide. | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_10_0_338_305 | The effects of mitiglinide (KAD-1229), a new anti-diabetic drug, on ATP-sensitive K+ channels and @GENE-Y$ secretion: comparison with the @CHEMICAL$ and nateglinide. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_10_0_306_337 | The effects of @CHEMICAL$ (KAD-1229), a new anti-diabetic drug, on @GENE-N$ and insulin secretion: comparison with the sulfonylureas and nateglinide. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_10_0_306_338 | The effects of @CHEMICAL$ (KAD-1229), a new anti-diabetic drug, on ATP-sensitive K+ channels and @GENE-Y$ secretion: comparison with the sulfonylureas and nateglinide. | [
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "head"
},
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_10_0_337_307 | The effects of mitiglinide (KAD-1229), a new anti-diabetic drug, on @GENE-N$ and insulin secretion: comparison with the sulfonylureas and @CHEMICAL$. | [
{
"text": "@GENE-N$",
"label": "GENE-N",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
}
] |
chemprot_train_10_0_338_307 | The effects of mitiglinide (KAD-1229), a new anti-diabetic drug, on ATP-sensitive K+ channels and @GENE-Y$ secretion: comparison with the sulfonylureas and @CHEMICAL$. | [
{
"text": "@GENE-Y$",
"label": "GENE-Y",
"role": "head"
},
{
"text": "@CHEMICAL$",
"label": "CHEMICAL",
"role": "tail"
}
] | [
{
"head": 0,
"tail": 1,
"label": "false"
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chemprot_train_10_0_308_337 | The effects of mitiglinide (@CHEMICAL$), a new anti-diabetic drug, on @GENE-N$ and insulin secretion: comparison with the sulfonylureas and nateglinide. | [
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chemprot_train_10_0_308_338 | The effects of mitiglinide (@CHEMICAL$), a new anti-diabetic drug, on ATP-sensitive K+ channels and @GENE-Y$ secretion: comparison with the sulfonylureas and nateglinide. | [
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chemprot_train_10_1_268_309 | @CHEMICAL$ (KAD-1229), a new anti-diabetic drug, is thought to stimulate insulin secretion by closing the @GENE-N$ in pancreatic beta-cells. | [
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chemprot_train_10_1_268_329 | @CHEMICAL$ (KAD-1229), a new anti-diabetic drug, is thought to stimulate @GENE-Y$ secretion by closing the ATP-sensitive K+ (K(ATP)) channels in pancreatic beta-cells. | [
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chemprot_train_10_1_309_270 | Mitiglinide (KAD-1229), a new anti-diabetic drug, is thought to stimulate insulin secretion by closing the @CHEM-GENE$ in pancreatic beta-cells. | [
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chemprot_train_10_1_329_270 | Mitiglinide (KAD-1229), a new anti-diabetic drug, is thought to stimulate @GENE-Y$ secretion by closing the @CHEMICAL$-sensitive K+ (K(ATP)) channels in pancreatic beta-cells. | [
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chemprot_train_10_1_309_275 | Mitiglinide (KAD-1229), a new anti-diabetic drug, is thought to stimulate insulin secretion by closing the @CHEM-GENE$ in pancreatic beta-cells. | [
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