目录号 | 产品详情 | 靶点 | |
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T64015 | |||
FGFR4-IN-6 是一种共价的、可逆的 FGFR4 抑制剂 (IC50: 5.4 nM),表现出良好的口服药代动力学特性。 在 Hep3B2.1-7 HCC 细胞系的异种移植小鼠模型中,FGFR4-IN-6 能够明显诱导肿瘤消退,且无明显的毒性。 | |||
T74749 | |||
AK-2292 是一种有效和选择性STAT5PROTAC 降解剂,DC50值为 0.10 μM。AK-2292 在体外和体内诱导 STAT5A/B 蛋白的降解。AK-2292 可在急性髓性白血病和慢性髓性白血病异种移植小鼠模型中诱导肿瘤消退。 | |||
T34278 | |||
Redaporfin, also known as F-2BMet or LUZ-11, is a photosensitizer for Photodynamic Therapy (PDT) of cancer. Redaporfin showed a high efficacy in the treatment of male BALB/c mice with subcutaneously implanted colon (CT26) tumours. Vascular-PDT with 1.5 mg | |||
T9684 | |||
(Z)-Orantinib ((Z)-SU6668) 是一种有效,选择性,具有口服活性和 ATP 竞争性的 Flk‐1/KDR,PDGFRβ和 FGFR1抑制剂,IC50值分别为 2.1,0.008 和 1.2 μM。(Z)-Orantinib 是有效的抗血管生成和抗肿瘤剂,可诱导已形成的肿瘤消退。 | |||
T18680 | Others | ||
SD-36, a potent and efficacious PROTAC STAT3 degrader (Kd=~50 nM), exhibits high specificity for STAT3 over other STAT members. It effectively targets both wild-type and mutated STAT3 proteins in cells, inhibiting their transcriptional activity (IC50=10 nM). The compound, consisting of the STAT3 inhibitor SI-109, a linker, and a CRBN ligand Lenalidomide analog for E3 ubiquitin ligase[1], demonstrates significant anti-tumor effects and achieves complete, long-lasting tumor regression in mouse models. | |||
T70588 | |||
Tazemetostat HCl is a potent, selective, and orally bioavailable small-molecule inhibitor of EZH2 enzymatic activity. EPZ-6438 induces apoptosis and differentiation specifically in SMARCB1-deleted MRT cells. Treatment of xenograft-bearing mice with EPZ-6438 leads to dose-dependent regression of MRTs with correlative diminution of intratumoral trimethylation levels of lysine 27 on histone H3, and prevention of tumor regrowth after dosing cessation. These data demonstrate the dependency of SMARCB1 mutant MRTs on EZH2 enzymatic activity and portend the utility of EZH2-targeted drugs for the treatment of these genetically defined cancers. | |||
T9429 | |||
ZZW-115 是一种有效的 NUPR1抑制剂,Kd 为 2.1 μM。ZZW-115是三氟拉嗪(TFP)的衍生物。ZZW-115显示出剂量依赖性肿瘤消退,无神经系统副作用,主要通过坏死和凋亡诱导细胞死亡。 | |||
T62847 | |||
AMXI-5001 是一种有效的、口服具有活力的 parp1/2 和微管聚合抑制剂。MXI-5001 对多种人类癌细胞显示出选择性抗肿瘤细胞毒性,其 IC50s 远低于现有的临床 PARP1/2 抑制剂。AMXI-5001 能够诱导已建立的肿瘤(包括很大的肿瘤)完全消退。 | |||
T78836 | PI3K | ||
IHMT-PI3K-455(Compound 15u)为一种高效、选择性且具口服活性的PI3Kγ/δ双重抑制剂,其针对PI3Kγ与PI3Kδ的IC50值分别为7.1 nM和0.57 nM。该化合物能够抑制AKT磷酸化,并通过促进CD8+杀伤性T细胞的招募与激活,抑制肿瘤生长,适用于肿瘤学研究领域。 | |||
T82517 | |||
DYSP-C34是一种生物相容性强且有效的超声(US)激活多功能分子机器。它提升了亲脂性/亲水性平衡,增强了超声诱导的ROS产生,并改善了细胞渗透能力,进而显著提升了对肿瘤的靶向效果及声动力疗法(SDT)介导的肿瘤缩减能力。此外,DYSP-C34还通过激活APC展示出温和的免疫原性。 |
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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