目录号 | 产品详情 | 靶点 | |
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T70133 | |||
BAY-846 is an allosteric MEK inhibitor with long half-lives, high bioavailabilities, low brain penetration potential and high efficacy in a K-Ras-mutated A549 xenograft model. | |||
T82108 | |||
ICMT-IN-35(即compound 10n),作为FTPA-triazole类ICMT抑制剂(IC50=0.8 μM),能被哺乳动物细胞吸收并阻断K-Ras膜定位,进而诱导K-Ras错定位。ICMT-IN-35对ICMT+/+MEF细胞表现出选择性细胞毒性,对转移性胰腺癌细胞系展示低微摩尔级别活性(IC50=0.8 μM)。 | |||
T72707 | |||
(Rac)-Lonafarnib (Sch66336外消旋体) 作为Lonafarnib的外消旋体,属于一种口服有效的法尼基蛋白转移酶 (FPTase) 抑制剂,针对H-ras、K-ras及N-ras展现出杰出的抑制效能,其IC50值分别为1.9 nM、5.2 nM和2.8 nM。此外,Lonafarnib还显示出对抗肝炎三角洲病毒 (HDV) 的潜在活性。 | |||
T18846 | Others | ||
THP-PEG4-Pyrrolidine(N-Boc)-CH2OH is a polyethylene glycol (PEG) based PROteolysis TArgeting Chimera (PROTAC) linker, employed for the synthesis of PROTAC K-Ras Degrader-1, as documented in reference [1]. | |||
T82086 | |||
ICMT-IN-7(化合物74)是一种高效的ICMT抑制剂,其IC50值为0.015 μM。该化合物能剂量依赖性地在HCT-116细胞中诱导ICMT蛋白在胞质的积累,并能抑制表达K-Ras和N-Ras的多种癌细胞系的增殖。 | |||
T82136 | |||
ICMT-IN-1 (化合物75) 作为一种高效的ICMT抑制剂展现出显著活性(IC50=0.0013 μM),能够剂量依赖性地在HCT-116细胞中导致ICMT的胞质内积累,进而有效抑制携带K-Ras和N-Ras变异的多个癌细胞系的增殖。 | |||
T74973 | |||
KRas G12R inhibitor 1 (compound 3) 是一种 KRas G12R 选择性共价抑制剂,可以利用突变半胱氨酸的强亲核性,在 K-Ras 的 Switch II 区域不可逆结合。KRas G12R inhibitor 1 可用于癌症研究。 | |||
T74920 | |||
G12Si-2,一种 G12Si-1 的类似物,可作为阴性对照。G12Si-2 不是 KRAS G12S 突变体的共价抑制剂。 | |||
T73822 | |||
GGTI-286 TFA 是一种高效的细胞通透性 GGTase I 抑制剂,(IC50为 2 μM。在 NIH3T3 细胞中,GGTI-286 TFA 对 Rap1A 香叶香叶基化的抑制作用高于 H-Ras 的法尼化作用 (IC50s=2 和 >30 μM)。GGTI-286 TFA 还能有效抑制 K-Ras4B 刺激,IC50为 1 μM。 | |||
T79464 | ROR | ||
RORγ antagonist1 (化合物22) 作为RORγ的有效拮抗剂 (KD=0.18 μM),在HPAF-II胰腺癌异种移植模型中显示出了抗增殖性能。该化合物通过抑制RAS/MAPK和AKT/mTORC1通路,并引发caspase依赖的细胞凋亡(apoptosis)机制,从而在胰腺癌细胞中发挥作用。 |
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-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-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-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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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-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-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-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-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-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-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-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-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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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-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-01439 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) 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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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-01400 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) 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.
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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-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-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-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-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-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-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-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-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-01405 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) 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-01443 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) 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. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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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-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-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-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-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-01525 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) 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-01427 | HLA-A*11:01&B2M&KRAS G12D (VVGADGVGK) 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-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-01403 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) 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-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-01404 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) 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-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-01402 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) 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-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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TMPK-01440 | HLA-A*11:01&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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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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