目录号 | 产品详情 | 靶点 | |
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T79461 | EGFR | ||
YK-029A为口服活性的EGFR突变抑制剂,特异性针对EGFRT790M及EGFRex20ins。该化合物在PDX模型上对肿瘤展现良好的抑制效果,显示出明显的抗肿瘤活性。 | |||
T71023 | |||
MI-888 is a potent MDM2 inhibitor (Ki = 0.44 nM) with a superior pharmacokinetic profile and enhanced in vivo efficacy. MI-888 is capable of achieving rapid, complete, and durable tumor regression in two types of xenograft models of human cancer with oral administration and represents the most potent and efficacious MDM2 inhibitor reported to date. | |||
T78442 | |||
TSPP tetrasodium 作为一种光敏剂, 在癌症与微生物感染治疗中展现出效用(Ex: 413 nm, Em: 640 nm)。 | |||
T32026 | |||
GYKI-13324 is bifunctional nitrosoureido derivative and alkylating agent. GYKI-13324 was studied on human colorectal tumor xenograft lines. Given orally in single or multiple daily doses, GYKI-13324 produced long-term or total regression of adenomatous, b | |||
T70356 | |||
F-1394 is an acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor. F-1394 both prevents the formation of atherosclerosis and accelerates its regression without affecting the serum TC level, indicating that F-1394 acts directly on the arterial wall. F-1394 significantly reduced neointimal thickening and the extent of macrophages in lesions without affecting serum cholesterol levels. In vitro, F-1394 attenuated foam cell formation in mouse peritoneal macrophages. | |||
T78211 | PI3K | ||
STX-478(化合物 80)为口服活性、能穿透血脑屏障、选择性针对突变型构象PI3Kα的抑制剂。STX-478表现出对肿瘤的强效抑制和长期缩减效果,适用于癌症研究。 | |||
T70552 | |||
Ipatasertib, also known as GDC0068, is an orally active, potent and selective Akt inhibitor. GDC-0068 blocked Akt signaling both in cultured human cancer cell lines and in tumor xenograft models. Inhibition of Akt activity by GDC-0068 resulted in blockade of cell-cycle progression and reduced viability of cancer cell lines. Markers of Akt activation, including high-basal phospho-Akt levels, PTEN loss, and PIK3CA kinase domain mutations, correlate with sensitivity to GDC-0068. In multiple tumor xenograft models, oral administration of GDC-0068 resulted in antitumor activity ranging from tumor growth delay to regression. | |||
T74975 | |||
Zn-DPA-maytansinoid conjugate 1 为一种靶向小分子免疫检查点的类美坦素偶联物。其能持续诱导肿瘤生长消退,并激活肿瘤微环境(TME),转化为“炎热肿瘤”。 | |||
T77115 | |||
Plamotamab (XmAb-13676) 是一种人源双特异性抗体(bsAb),目标是CD3和CD20,通过招募细胞毒性T细胞以消灭CD20+表达的肿瘤细胞。在体内,Plamotamab诱导了轻微的血液学反应(MR)并有效促进肿瘤消退。 | |||
T36201 | |||
Dimeric Smac mimetic; potent inhibitor of X-linked (XIAP) and cellular (cIAP) inhibitor of apoptosis protein (IC50 values are 15, 15 and 21 nM for XIAP, cIAP1 and cIAP2 respectively). Binds to the BIR3 domain of XIAP to prevent interaction with caspase-9. Causes degradation of cIAP1 and cIAP2 and induces apoptosis in MDA-MB-231 breast cancer cells. Causes tumor regression in MDA-MB-231 xenograft-bearing mice. Hennessy et al (2013) Discovery of a novel class of dimeric Smac mimetics as potent IAP antagonists resulting in a clinical candidate for the treatment of cancer (AZD5582). J.Med.Chem. 56 9897 PMID:24320998 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-05176 | AMH Protein, Human, Recombinant (His) | Human | HEK293 | ||
Anti-Mullerian hormone (AMH), a member of the TGF-beta superfamily, is produced by granulosa cells (GCs) of preantral and small antral follicles and plays a role in regulating the recruitment of primordial follicles and the FSH-dependent development of follicles. BMP15 up-regulates the transcription of AMH and that the inhibition of p38 MAPK decreases the BMP15-induced expression of AMH and SOX9, suggesting that BMP15 up-regulates the expression of AMH via the p38 MAPK signaling pathway, and this process involves the SOX9 transcription factor. AMH is widely used for assessing ovarian reserve, and it is particularly convenient, because it is thought to have minimal variability throughout the menstrual cycle. Fetal anti-Mullerian hormone (AMH) is responsible for normal male sexual differentiation, and circulating AMH is used as a marker of testicular tissue in newborns with disorders of sex development. Anti-Mullerian hormone (AMH) produced in the developing testis induces the regression of the Mullerian duct, which develops into the oviducts, uterus and upper vagina. As well as other hormone receptors, and a decreased ovarian cortex cell proliferation. These results help understand the inhibitory effects of AMH on follicular development.
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TMPH-01201 | DRD2 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Dopamine receptor whose activity is mediated by G proteins which inhibit adenylyl cyclase. Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5.
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TMPH-01335 | FGF-5 Protein, Human, Recombinant (GST & His & Myc) | Human | E. coli | ||
Plays an important role in the regulation of cell proliferation and cell differentiation. Required for normal regulation of the hair growth cycle. Functions as an inhibitor of hair elongation by promoting progression from anagen, the growth phase of the hair follicle, into catagen the apoptosis-induced regression phase.
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TMPH-02654 | FGF-5 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Plays an important role in the regulation of cell proliferation and cell differentiation. Required for normal regulation of the hair growth cycle. Functions as an inhibitor of hair elongation by promoting progression from anagen, the growth phase of the hair follicle, into catagen the apoptosis-induced regression phase.
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TMPH-03241 | Angiopoietin-2 Protein, Rat, Recombinant (E. coli, His) | Rat | E. coli | ||
Binds to TEK/TIE2, competing for the ANGPT1 binding site, and modulating ANGPT1 signaling. Can induce tyrosine phosphorylation of TEK/TIE2 in the absence of ANGPT1. In the absence of angiogenic inducers, such as VEGF, ANGPT2-mediated loosening of cell-matrix contacts may induce endothelial cell apoptosis with consequent vascular regression. In concert with VEGF, it may facilitate endothelial cell migration and proliferation, thus serving as a permissive angiogenic signal.
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TMPH-03240 | Angiopoietin-2 Protein, Rat, Recombinant (His) | Rat | Baculovirus | ||
Binds to TEK/TIE2, competing for the ANGPT1 binding site, and modulating ANGPT1 signaling. Can induce tyrosine phosphorylation of TEK/TIE2 in the absence of ANGPT1. In the absence of angiogenic inducers, such as VEGF, ANGPT2-mediated loosening of cell-matrix contacts may induce endothelial cell apoptosis with consequent vascular regression. In concert with VEGF, it may facilitate endothelial cell migration and proliferation, thus serving as a permissive angiogenic signal.
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TMPJ-01114 | GAMT Protein, Human, Recombinant (His) | Human | E. coli | ||
GAMT is a methyltransferase which belongs to the class I-like SAM-binding methyltransferase superfamily. It contains one RMT2 (arginine N-methyltransferase 2-like) domain and is expressed in liver. GAMT converts guanidoacetate to creatine, using S-adenosylmethionine as the methyl donor. Defects in GAMT are the cause of guanidinoacetate methyltransferase deficiency, which is an autosomal recessive disorder characterized by developmental delay/regression, mental retardation, severe disturbance of expressive and cognitive speech, intractable seizures and movement disturbances, severe depletion of creatine/phosphocreatine in the brain, and accumulation of guanidinoacetic acid in brain and body fluids.
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TMPH-00279 | Interferon tau-1/IFNT1 Protein, Bovine, Recombinant (His) | Bovine | Yeast | ||
Paracrine hormone primarily responsible for maternal recognition of pregnancy. Interacts with endometrial receptors, probably type I interferon receptors, and blocks estrogen receptor expression, preventing the estrogen-induced increase in oxytocin receptor expression in the endometrium. This results in the suppression of the pulsatile endometrial release of the luteolytic hormone prostaglandin F2-alpha, hindering the regression of the corpus luteum (luteolysis) and therefore a return to ovarian cyclicity. This, and a possible direct effect of IFN-tau on prostaglandin synthesis, leads in turn to continued ovarian progesterone secretion, which stimulates the secretion by the endometrium of the nutrients required for the growth of the conceptus. In summary, displays particularly high antiviral and antiproliferative potency concurrently with particular weak cytotoxicity, high antiluteolytic activity and immunomodulatory properties. In contrast with other IFNs, IFN-tau is not virally inducible.
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TMPH-00278 | Interferon tau-1/IFNT1 Protein, Bovine, Recombinant (E. coli, His) | Bovine | E. coli | ||
Paracrine hormone primarily responsible for maternal recognition of pregnancy. Interacts with endometrial receptors, probably type I interferon receptors, and blocks estrogen receptor expression, preventing the estrogen-induced increase in oxytocin receptor expression in the endometrium. This results in the suppression of the pulsatile endometrial release of the luteolytic hormone prostaglandin F2-alpha, hindering the regression of the corpus luteum (luteolysis) and therefore a return to ovarian cyclicity. This, and a possible direct effect of IFN-tau on prostaglandin synthesis, leads in turn to continued ovarian progesterone secretion, which stimulates the secretion by the endometrium of the nutrients required for the growth of the conceptus. In summary, displays particularly high antiviral and antiproliferative potency concurrently with particular weak cytotoxicity, high antiluteolytic activity and immunomodulatory properties. In contrast with other IFNs, IFN-tau is not virally inducible.
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TMPY-01924 | HSP60 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
HSPD1, also known as HSP60, is a member of the chaperonin family. HSPD1 may function as a signaling molecule in the innate immune system. This protein is essential for the folding and assembly of newly imported proteins in the mitochondria. It may also prevent misfolding and promote the refolding and proper assembly of unfolded polypeptides generated under stress conditions in the mitochondrial matrix. HSPD1 gene is adjacent to a related family member and the region between the 2 genes functions as a bidirectional promoter. Several pseudogenes have been associated with this gene. Mutations associated with this gene cause autosomal recessive spastic paraplegia 13. Defects in HSPD1 are a cause of spastic paraplegia autosomal dominant type 13 (SPG13). Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Defects in HSPD1 are the cause of leukodystrophy hypomyelinating type 4 (HLD4); also called mitochondrial HSP60 chaperonopathy or MitCHAP-60 disease. HLD4 is a severe autosomal recessive hypomyelinating leukodystrophy. HSPD1 is clinically characterized by infantile-onset rotary nystagmus, progressive spastic paraplegia, neurologic regression, motor impairment, profound mental retardation. Death usually occurs within the first two decades of life.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01876 | HSP60 Protein, Human, Recombinant (His & GST) | Human | E. coli | ||
HSPD1, also known as HSP60, is a member of the chaperonin family. HSPD1 may function as a signaling molecule in the innate immune system. This protein is essential for the folding and assembly of newly imported proteins in the mitochondria. It may also prevent misfolding and promote the refolding and proper assembly of unfolded polypeptides generated under stress conditions in the mitochondrial matrix. HSPD1 gene is adjacent to a related family member and the region between the 2 genes functions as a bidirectional promoter. Several pseudogenes have been associated with this gene. Mutations associated with this gene cause autosomal recessive spastic paraplegia 13. Defects in HSPD1 are a cause of spastic paraplegia autosomal dominant type 13 (SPG13). Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Defects in HSPD1 are the cause of leukodystrophy hypomyelinating type 4 (HLD4); also called mitochondrial HSP60 chaperonopathy or MitCHAP-60 disease. HLD4 is a severe autosomal recessive hypomyelinating leukodystrophy. HSPD1 is clinically characterized by infantile-onset rotary nystagmus, progressive spastic paraplegia, neurologic regression, motor impairment, profound mental retardation. Death usually occurs within the first two decades of life.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPJ-00303 | ANG2 Protein, Mouse, Recombinant (hFc) | Mouse | Human Cells | ||
Angiopoietin-2 (Ang-2; also ANGPT2) is a secreted glycoprotein that plays a complex role in angiogenesis and inflammation. Both Ang-2 and the related Angiopoietin-1 (Ang-1) are ligands for the receptor tyrosine kinase Tie-2. While Ang-1 is a potent Tie 2 agonist, Ang-2 may act as either a Tie-2 antagonist or agonist, depending upon its state of multimerization. The higher the order of oligomer, the more effective Ang-2 becomes as a Tie-2 agonist. The short isoform appears to block the binding of either Ang-1 or full-length Ang-2 to Tie-2. Ang-2 functions as a pro-angiogenic factor, although it can also induce EC death and vessel regression. Upon its release from quiescent EC, it regulates vascular remodeling by promoting EC survival, proliferation, and migration and destabilizing the interaction between EC and perivascular cells. In addition, ANG-2 is strongly expressed in the vasculature of many tumors and it has been suggested that ANG-2 may act synergistically with other cytokines such as vascular endothelial growth factor to promote tumor-associated Angiogenesis and tumor progression.
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TMPJ-01435 | ANG2 Protein, Rhesus macaque, Recombinant (hFc) | Rhesus Macaque | Human Cells | ||
Angiopoietin-2 (Ang-2; also ANGPT2) is a secreted glycoprotein that plays a complex role in angiogenesis and inflammation. Both Ang-2 and the related Angiopoietin-1 (Ang-1) are ligands for the receptor tyrosine kinase Tie-2. While Ang-1 is a potent Tie 2 agonist, Ang-2 may act as either a Tie-2 antagonist or agonist, depending upon its state of multimerization. The higher the order of oligomer, the more effective Ang-2 becomes as a Tie-2 agonist. The short isoform appears to block the binding of either Ang-1 or full-length Ang-2 to Tie-2. Ang-2 functions as a pro-angiogenic factor, although it can also induce EC death and vessel regression. Upon its release from quiescent EC, it regulates vascular remodeling by promoting EC survival, proliferation, and migration and destabilizing the interaction between EC and perivascular cells. In addition, ANG-2 is strongly expressed in the vasculature of many tumors and it has been suggested that ANG-2 may act synergistically with other cytokines such as vascular endothelial growth factor to promote tumor-associated Angiogenesis and tumor progression.
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