目录号 | 产品详情 | 靶点 | |
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T6266L | |||
PP2 Analog is an analog of PP2. It also acts as a protein trafficking modulator. | |||
T11256 | FAAH | ||
FAAH inhibitor 1 (Benzothiazole analog 3) 是一种有效的脂肪酸酰胺水解酶抑制剂,IC50 为 18 nM。 | |||
T2153 | Serine/threonin kinase CDK Src | ||
1-NM-PP1 (PP1 Analog II) 是一种有效的Src 家族激酶抑制剂,是一种细胞渗透性 PP1 类似物,对 v-Src-as1 与 c-Fyn-as1 的IC50值分别为 4.3 nM、3.2 nM。 | |||
T11916 | Bcr-Abl Src | ||
Lyn-IN-1 (Bafetinib analog) 是一种高活性 Bcr-Abl 和 Lyn 双重抑制剂。 | |||
T65550 | Others | ||
Gefitinib analog III (4-((3-Chloro-4-fluorophenyl)amino)-7-methoxyquinazolin-6-yl acetate) 具有潜在的抗炎和抗肿瘤活性,可用于研究其在生物体内的相互作用和活性。 | |||
T3059 | EGFR IGF-1R ALK | ||
ALK-IN-1 (AP26113) 是一种高效的、选择性的 ALK 激酶抑制剂。 | |||
T38551 | |||
Liproxstatin-1 analog is a potent ferroptosis inhibitor, derived from liproxstatin-1 with a similar structure. It effectively inhibits ferroptotic cell death, with an IC50 value of 22 nM. | |||
T39606 | |||
CE3F4 analog 1 is an analogue of CE3F4. | |||
T35747 | |||
Quinacrine is a compound with multiple actions that is commonly used as an anti-protozoal agent. It has also been shown to be a highly potent autophagy inhibitor, although the dose required to achieve this effect is considerably cytotoxic (LD50 = 2.5 μM). Quinacrine analog 34 is a derivative of quinacrine that was designed with an improved cell viability profile (LD50 = 27 μM) to inhibit autophagy. At a minimum concentration of 0.5 μM, this compound has been shown to increase the protein levels of the autophagy biomarker LC3-II and to induce lysosome deacidification. | |||
T16162 | EGFR | ||
Mutated EGFR-IN-1 (Osimertinib analog) 是用于突变 EGFR 抑制剂设计的有用中间体,例如 L858R EGFR、Exon19 缺失激活突变体和 T790M 抗性突变体。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-03036 | Cytotoxin 2 Protein, Naja atra, Recombinant (His & Myc) | Naja atra | E. coli | ||
Basic protein that binds to cell membrane and depolarizes cardiomyocytes. It also shows lytic activities, but 2-fold less important than that of CTX-A4. It binds to the integrin alpha-V/beta-3 (ITGAV/ITGB3) with a moderate affinity. It may interact with sulfatides in the cell membrane which induces pore formation and cell internalization and is responsible for cytotoxicity in cardiomyocytes. It also may target the mitochondrial membrane and induce mitochondrial swelling and fragmentation.
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TMPH-00645 | Lactose permease Protein, E. coli, Recombinant (His) | E. coli | in vitro E. coli expression system | ||
Responsible for transport of beta-galactosides into the cell, with the concomitant import of a proton (symport system). Can transport lactose, melibiose, lactulose or the analog methyl-1-thio-beta,D-galactopyranoside (TMG), but not sucrose or fructose. The substrate specificity is directed toward the galactopyranosyl moiety of the substrate.
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TMPJ-00871 | BAR Protein, S. hygroscopicus, Recombinant | Streptomyces hygroscopicus | E. coli | ||
Phosphinothricin N-acetyltransferase (PAT) is an enzyme that acetylates the free NH2 group of L-phosphinothricin (L-PPT) in the presence of acetyl-CoA as a co-substrate. It is highly specific for L-PPT and does not acetylate other L-amino acids or structurally similar molecules. L-PPT is a glutamate analog that can inhibit glutamine synthetase activity in plants, resulting in the accumulation of ammonia to toxic levels and impairment of photosynthesis. The introduction of a PAT gene into a plant genome can confer resistance to glufosinate herbicide during post-emergent applications.
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TMPH-03038 | Cobra venom factor Protein, Naja kaouthia, Recombinant (His & SUMO) | Naja kaouthia | E. coli | ||
Complement-activating protein in cobra venom. It is a structural and functional analog of complement component C3b, the activated form of C3. It binds factor B (CFB), which is subsequently cleaved by factor D (CFD) to form the bimolecular complex CVF/Bb. CVF/Bb is a C3/C5 convertase that cleaves both complement components C3 and C5. Structurally, it resembles the C3b degradation product C3c, which is not able to form a C3/C5 convertase. Unlike C3b/Bb, CVF/Bb is a stable complex and completely resistant to the actions of complement regulatory factors H (CFH) and I (CFI). Therefore, CVF continuously activates complement resulting in the depletion of complement activity.
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