目录号 | 产品详情 | 靶点 | |
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TP1289 | Others | ||
Cardiotoxin Analog (CTX) IV (6-12) TFA(115722-23-1 free base) 是 Cardiotoxin Analog (CTX) IV 的部分肽。从台湾眼镜蛇毒液中分离出的心脏毒素类似物 IV。 CTX IV 是一种独特的蛇毒心脏毒素。 | |||
T6351 | Apoptosis VEGFR c-Met/HGFR | ||
MGCD-265 analog (Glesatinib) 是一种口服生物可利用的多靶点酪氨酸激酶抑制剂,具有抗肿瘤活性,对 c-Met 和 VEGFR2 的 IC50 分别为 29 nM 和 10 nM。 | |||
T35450 | |||
α-Galactosylceramide analog 8 (α-GalCer analog 8) is a triazole derivative of α-galactosylceramide. [1] It increases IL-2 secretion by DN32.D3 NKT hybridoma cells when co-cultured with CD1d-transfected RBL cells pre-loaded with α-GalCer analog 8 at a concentration of 32 ng/ml. α-GalCer analog 8 (32 ng/ml) induces IL-4 secretion to a greater extent than the synthetic α-GalCer KRN 7000 in mouse splenocytes in vitro and in mouse serum following administration of a 1 µg per animal dose, indicating a Th2 response. | |||
T40156 | |||
MRTX849 analog 24 is an alkyne-containing click probe analogue of the MRTX849 inhibitor for KRAS G12C. It is specifically designed for studying the functionality of MRTX849. | |||
T3558 | EGFR | ||
EBE-A22 (PD153035 Analog 63) 是 PD153035 衍生物,PD153035 能够抑制 ErbB-1 磷酸化,但对 EBE-A22 则无抑制作用。 | |||
T78984 | ROS | ||
Xanthine oxidase-IN-10 (XO8 analog) 是一种黄嘌呤氧化酶 (XO) 抑制剂,可用于研究痛风。 | |||
T19519 | Others | ||
Pimelic Diphenylamide 106 analog is an Pimelic Diphenylamide 106 analog . | |||
T28919 | |||
Tamoxifen analog II is a potent growth inhibitor. Tamoxifen analog II displays activity against various cancer cell lines. | |||
T10629 | BTK | ||
Btk inhibitor 2 (BGB-3111 analog) 是一种布鲁顿酪氨酸激酶 (BTK) 抑制剂。 | |||
TQ0230 | BTK | ||
BTK IN-1 (SNS062 analog) (SNS062 analog) 是一种有效的 BTK 抑制剂 (IC50<100 nM)。 |
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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