目录号 | 产品详情 | 靶点 | |
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T77805 | |||
T11738 | Ras | ||
K-Ras G12C-IN-4 是一种 KRAS G12C 共价抑制剂。 | |||
T8418 | Others | ||
DCLK1-IN-1 是选择性的、体内相容的双皮质素样激酶1DCLK1激酶结构域化学探针。它抑制 DCLK1 和 DCLK2 激酶。它具有低毒性,可以研究 DCLK1 的生物学特性,确定其在肿瘤中的作用,如 DCLK1+胰腺导管腺癌。 | |||
T7414 | Apoptosis Raf Ras | ||
ARS-853 是一种选择性共价KRAS G12C 抑制剂,IC50为 2.5 μM。它通过与 GDP 结合的癌蛋白结合并阻止激活来抑制突变 KRAS 驱动的信号传导。 | |||
T16143 | Ras | ||
MRTX-1257 是选择性的、可口服的不可逆共价KRAS G12C 抑制剂,其在 H358 细胞中测得 KRAS 依赖 ERK 磷酸化的IC50值为 900 pM。 | |||
T12979 | p38 MAPK MAPK Ras | ||
BI-3406 是一种可口服、高效且选择性的 KRAS-SOS1 抑制剂,具有抗癌活性。它有效减少 GTP 加载的 KRAS 的形成,抑制 MAPK 信号通路。它还抑制 KRAS 与 SOS1之间相互作用,IC50为 6 nM。 | |||
T9303 | Ras | ||
MRTX1133 是一种 KRAS G12D 抑制剂 (KD=0.2 pM),具有强效性、选择性和非共价性。MRTX1133 对 KRAS G12D 突变的肿瘤具有抑制活性,而对 KRAS 野生型肿瘤无抑制活性。 | |||
T11224 | ERK Raf | ||
Rineterkib (ERK-IN-1) 是口服有效的RAF 和ERK1/2的抑制剂,与 KRAS-突变型非小细胞肺癌、BRAF-突变型非小细胞肺癌、KRAS-突变型胰腺癌、KRAS -突变型结肠癌和 KRAS-突变型卵巢癌尤为相关。 | |||
T8684 | Ras | ||
Sotorasib (AMG-510) 是一种 KRAS G12C 共价抑制剂,具有口服活性和选择性。Sotorasib 与 KRAS G12C 非活性构象的 GDP 状态结合,抑制 KRAS 及其下游信号的传导。Sotorasib 对 KRAS G12C 突变肿瘤具有抑制活性。 | |||
T11282 | Transferase | ||
FGTI-2734 是 有效的RAS C-末端法尼基转移酶 (FT) 和香叶烯基转移酶-1 (GGT-1) 抑制剂,IC50s 分别为 250 nM 和 520 nM。 它可以阻断 KRAS 的膜定位,从而解决 KRAS 耐药性问题,并抑制突变的 KRAS 胰腺肿瘤。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-06056 | KRAS Protein, Human, Recombinant (G12D, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01888 | KRAS Protein,Human, Recombinant (Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-04113 | KRAS Protein,Human,Recombinant(G12D & Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-04116 | KRAS Protein,Human,Recombinant(G12C & Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPJ-00511 | KRAS Protein, Human, Recombinant (G12V, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. As other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.
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TMPJ-00510 | KRAS Protein, Human, Recombinant (G12C, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. As other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.
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TMPY-06345 | KRAS Protein, Human, Recombinant (His & Avi), Biotinylated | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPK-01510 | HLA-A*03:01&B2M&KRAS WT (VVVGAGGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01488 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPY-06138 | KRAS Protein, Human, Recombinant (61Q, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPU-00001 | KRAS Protein, Human, Recombinant (G12S, GST) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. As other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.
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TMPK-01458 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01512 | HLA-A*03:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01529 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01463 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01527 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01518 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01433 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01401 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi) | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01451 | HLA-C 03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01489 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01511 | HLA-A*03:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01432 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01408 | HLA-A*02:01&B2M&KRAS G12V (KLVVVGAVGV) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01507 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01465 | HLA-A*11:01&B2M&KRAS G12R (VVVGARGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01528 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01407 | HLA-A*02:01&B2M&KRAS WT (KLVVVGAGGV) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01479 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01399 | HLA-A*11:01&B2M&KRAS WT (VVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01428 | HLA-A*11:01&B2M&KRAS G12D (VVGADGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01438 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Tetramer Protein, Human, MHC (His & Avi), PE-Labeled | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01456 | HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01460 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01462 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01490 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01431 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01526 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01434 | HLA-A*11:01&B2M&KRAS G12R (VVVGARGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01461 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01429 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01457 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01471 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), FITC-Labeled | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01450 | HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01464 | HLA-A*11:01&B2M&KRAS G12R (VVVGARGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01537 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01453 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01536 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01430 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi) | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01435 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Tetramer Protein, Human, MHC (His & Avi), PE-Labeled | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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