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Request The Product List ofHeat Shock Protein (HSP) Heat Shock Protein (HSP)

HSP (Heat shock proteins) are a group of proteins induced by heat shock, the most prominent members of this group are a class of functionally related proteins involved in the folding and unfolding of other proteins. HSP expression is increased when cells are exposed to elevated temperatures or other stress. This increase in expression is transcriptionally regulated. The dramatic upregulation of the heat shock proteins is a key part of the heat shock response and is induced primarily by heat shock factor (HSF). HSPs are found in virtually all living organisms, from bacteria to humans. Heat shock proteins appear to serve a significant cardiovascular role. Hsp90, Hsp84, Hsp70, Hsp27, Hsp20 and alpha B crystallin all have been reported as having roles in the cardiovasculature.

Cat. No. Product Name CAS No. Information



A potent, orally available Pirin ligand (Ki=28 nM), blocks the HSF1-mediated induction of both HSP72 and HSP27; inhibits the induction of HSP72 at the mRNA level, blocks the induction of HSPA1A gene expression with IC50 of 40 nM, inhibits SK-OV-3 cells proliferation with GI50 of 1.1 nM; displays efficacy in a human ovarian carcinoma xenograft model.




A potent and selective Grp94 inhibitor with Ic50 of 0.22 uM; shows >35 fold selectivity over other four HSP90 paralogs, Hsp90α, Hsp90β and Trap-1 (IC50> 7 uM).




YZ129 (YZ-129) is a small molecule inhibitor of HSP90-Calcineurin-NFAT pathway, suppresses TG-induced NFAT nuclear translocation in HeLa cellswith IC50 of 820 nM; also suppressed the expression of NFAT-regulated genes, such as COX2, MMP7, and MMP9, in U87 GBM cells; directly binds to HSP90 to antagonize its chaperoning effect on calcineurin, a Ca2+-sensitive phosphatase that is required for NFAT nuclear translocation and subsequent gene expression; YZ129 could not only suppress cancer cell growth but also reduce cancer cell movement and migration of of GBM cells in vitro; suppresses the growth of GBM xenografts in vivo.




JG-231 is an allosteric inhibitor that disrupts the Hsp70-BAG3 interaction (Ki=0.11 uM), inhibits breast cancer cells MCF-7 and MDA-MB-231 with IC50 of 0.12 and 0.25 uM, respectively; reduces tumor burden in an MDA-MB-231 xenograft model (4 mg/kg, ip).




HSP70-IN-27c is a potent, irreversible inhibitor of Hsp70 without Hsp 90 binding activity, inhibits growth of Kasumi-1 AML cells with IC50 of 2.3 uM, and inhibits Caspase-3,7 activation in MOLM13 AML cells with IC50 of 1.9 uM; inhibits HER2 and Raf-1 steady-state levels, PARP cleavage in SKBr3 breast cancer cells with IC50 of about 1.5 uM, induces apoptosis in MDA-MB-468 cells.




A small molecule human HSF1 (heat shock transcription factor 1) activator; activates HSF1 in mammalian and fly cells, elevates protein chaperone expression, ameliorates protein misfolding and cell death in polyQ-expressing neuronal precursor cells and protects against cytotoxicity in a fly model of polyQ-mediated neurodegeneration; also interacts with components of the TRiC/CCT complex.


PF-04929113 Mesylate


The prodrug of PF-04928473 (SNX-2112), a potent, orally bioavailable HSP90 inhibitor; inhibits several signaling pathways and induces apoptosis in CRPC LNCaP tumors in vivo.




A novel activator of HSP70 with EC50 of 4.6 uM; induces HSF-1-dependent chaperone expression and restores protein folding in conformational disease models, which are mediated by novel mechanisms involving FOXO, HSF-1, and Nfr-2.




An inhibitor of Heat shock protein (HSP) synthesis that dose-dependently inhibits the acquisition of thermotolerance and the induction of various HSPs including HSP105, HSP70, and HSP40 in human colon carcinoma cells; inhibits the acquisition of thermotolerance as developed by sodium arsenite, also inhibited at mRNA levels; shows no antitumor effects and does not increase the thermosensitivity of nontolerant tumors in vivo (up to 200 mg/kg).


Tanespimycin hydrochloride


A potent Hsp90 inhibitor with IC50 of 5 nM in cell-free assays; induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells; causes the degradation of HER2, HER3, Akt, and both mutant and wild-type androgen receptor; inhibits prostate cancer xenografts growth in mice.

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