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Serine Hydrolase inhibitor-21 (compound 8), a pyridine, is a serine hydrolaseinhibitor with a Ki of 429 nM for BuChE. Serine Hydrolase inhibitor-21 has the potential for Alzheimer's disease research [1].
PROTAC Mcl1degrader-1 (compound C3), a proteolysis targeting chimera (PROTAC) based on Cereblon ligand, is a potently and selectively Mcl-1 (Bcl-2 family member) inhibitor with an IC50 of 0.78 μM. PROTAC Mcl1degrader-1inhibitsBcl-2 with an IC50 of 0.54 μM [1].
Mcl-1inhibitor 21 (Example 1-36) is a Mcl-1inhibitor with an IC50 of 328 nM. Mcl-1inhibitor 21 exhibits proapototic and anti-proliferation activities against SUDHL5 and SUDHL10 cell lines and can be utilized in cancer research [1].
(-)-Mcl-1inhibitor 21 (Example 1-38) is a Mcl-1inhibitor with an IC50 of 7.51 μM. (-)-Mcl-1inhibitor 21 exhibits proapototic and anti-proliferation activities against SUDHL5 and SUDHL10 cell lines and can be utilized in cancer research [1].
(+)-Mcl-1inhibitor 21 (Example 1-37) is a Mcl-1inhibitor with an IC50 of 172 nM. (+)-Mcl-1inhibitor 21 exhibits proapototic and anti-proliferation activities against SUDHL5 and SUDHL10 cell lines and can be utilized in cancer research [1].
HIV-1inhibitor-21 (compound 9b) is a potent HIV-1 non-nucleoside reverse transcriptase (RT) inhibitor, with an IC50 value of 0.55 μM for HIV-1 RT. HIV-1inhibitor-21 has antiretroviral activity against HIV-1 WT and K103N strains with EC50s of 12.7 nM and 10.4 nM, and has relatively low cytotoxicity (MT-4 cells CC50 =10.2 μM) [1].
Mcl-1inhibitor 10 (compound 43) is a relatively strong MCL-1inhibitor (IC50=0.67 μM). Mcl-1inhibitor 10 interacts with specific binding sites of MCL-1 protein to block the pro-survival signal of MCL-1 and push cancer cells into apoptosis. Mcl-1inhibitor 10 can be used in the study of MCL-1 dependent cancers [1].
(-)-Mcl-1inhibitor 22 (compound 38) is an Mcl-1inhibitor that works by blocking the interaction between Mcl-1 and pro-apoptotic proteins, reducing the anti-apoptotic activity of Mcl-1. (-)-Mcl-1inhibitor 22 can be used in cancer research [1].
Mcl-1inhibitor 20 (compound 47) is a Mcl-1inhibitor with anti-leukemic effects. Mcl-1inhibitor 20 can bind to the BH3 binding groove of Mcl-1 (Ki=24 nM), occupy the P1 pocket in Mcl-1, and form interactions with Lys234 and Val249. Mcl-1inhibitor 20 has good microsomal stability, pharmacokinetic characteristics and low cardiotoxicity [1].
Mcl-1inhibitor 9 (example 2) is a myeloid cell leukemia 1(Mcl-1)inhibitor with IC50 value of 0.21889 nM. Mcl-1inhibitor 9 shows anti-tumor activity [1].
Mcl-1inhibitor 16 (Compound 9) is a mitochondrial targeting Platinum-based inhibitor of Mcl-1. Mcl-1inhibitor1 induces Bax/Bak-dependent apoptosis in cancer cells. Mcl-1inhibitor 16 can be used alone or together with ABT-199 (HY-15531) and shows anti-tumor activity [1].
Mcl-1inhibitor 22 (Example 36) is a myeloid cell leukemia-1 (MCL-1) inhibitor which inhibits the antiapoptotoic activity of MCL-1 by inhibiting its interaction with proapototic proteins. Mcl-1inhibitor 22 exhibits anti-proliferation activities against various cancer cell lines and can be utilized in cancer research [1].
(+)-Mcl-1inhibitor 22 (Example 37) is a myeloid cell leukemia-1(MCL-1)inhibitor which inhibits the antiapoptotoic activity of MCL-1 by inhibiting its interaction with proapototic proteins. (+)-Mcl-1inhibitor 22 exhibits anti-proliferation activities against various cancer cell lines and can be utilized in cancer research [1].
Mcl-1inhibitor 6 is an orally active, selective myeloid cell leukemia 1(Mcl-1) protein inhibitor with a Kd of 0.23 nM and a Ki of 0.02 μM. Mcl-1inhibitor 6 possesses superior selectivity over other Bcl-2 family members (Bcl-2, Bcl2A1, Bcl-xL, and Bcl-w, Kd>10 μM). Mcl-1inhibitor 6 is a potent antitumor agent [1].
Mcl-1inhibitor 3 (compound 1) is a highly potent and orally activate macrocyclic Mcl-1inhibitor (Ki= 0.061 nM; IC50=19 nM in an OPM-2 cell viability assay). Mcl-1inhibitor 3 shows good pharmacokinetic properties and excellent in vivo efficacy without toxicity [1]..
Mcl-1inhibitor 14 (Compound (Ra)-10) is an inhibitor of myeloid cell leukemia-1(MCL-1) with an Ki of 0.018 nM and can be used for anticancer research [1].
Mcl1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Mcl1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
MCL1 Human Pre-designed siRNA Set A contains three designed siRNAs for MCL1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Mcl1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Mcl1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
Tubulin inhibitor 21 (compound 6f), a chalcone- and melatonin- based hybrid, is a potent tubulininhibitor. Tubulin inhibitor 21 induces a remarkable cytotoxic activity toward SW480 cells (IC50=0.26 μM) with lower effect against nonmalignant cells [1].
Carbonic anhydrase inhibitor 21 (Compound 5h) is a selective carbonic anhydrase (hCA IX)inhibitor, with a Ki of 15.1?nM, and is highly selective against other investigated isoform. Carbonic anhydrase inhibitor 21 can be used for anticancer research [1].
P-gp inhibitor 21 (Compound 56) is an inhibitor for P-glycoprotein (P-gp) transport, which reverses P-gp-mediated multidrug resistance (MDR) and exhibits antitumor efficacy in mice without significant cytotoxicity [1].
GSK-3β inhibitor 21 (compound 44) is an ATP-competitive GSK-3βinhibitor (IC50=6.06 μM) with anti-amyloid aggregation and tau phosphorylation inhibitory activities. GSK-3β inhibitor 21 can be used in the study of Alzheimer's disease [1].
Mcl1-IN-14 (compound 5) is a reversible covalent inhibitor of Mcl-1 with the activity of inhibitingMcl-1. Mcl1-IN-14 covalently targets the non-catalytic lysine side chain of Mcl-1 and has higher potency than non-covalent counterparts, which can be used to develop Mcl-1 inhibitory compounds and study related biological phenomena.
Mcl1-IN-7 (compound 11) is a reversible covalent inhibitor of Mcl-1 with the activity of inhibitingMcl-1. By covalently targeting the non-catalytic lysine side chain of Mcl-1, it has higher potency than non-covalent counterparts and can be used to develop Mcl-1 inhibitory compounds and study related biological phenomena.
Mcl1-IN-15 (Compound 7) is the inhibitor for myeloid cell leukemia 1(Mcl-1) with an IC50 of 8.73 μM. Mcl1-IN-15 inhibitsMcl1-BH3 peptide interaction, activates the Bak/Bax-mediated apoptosis and exhibits antitumor activity [1].
Bcl-2/Mcl-1-IN-2 (compound 2) is a Bcl-2/Mcl-1inhibitor, with Kis of 0.88 μM and 4.70 μM for Mcl-1 and Bcl-2, respectively. Bcl-2/Mcl-1-IN-2 can be used for the research of cancer [1].
Bcl-2/Mcl-1-IN-1 (compound 3) is a Bcl-2/Mcl-1inhibitor, with Kis of 1.19 μM and 4.53 μM for Mcl-1 and Bcl-2, respectively. Bcl-2/Mcl-1-IN-1 can be used for the research of cancer [1].
Bcl-2/Mcl-1-IN-3 (compound 1) is a Bcl-2/Mcl-1inhibitor, with Kis of 0.14 μM and 0.23 μM for Mcl-1 and Bcl-2, respectively. Bcl-2/Mcl-1-IN-3 can be used for the research of cancer [1].
Icovamenib (BMF-219) is a selective, orally active, irreversible Menininhibitor. Icovamenib forms a stable and irreversible covalent bond with Menin. Icovamenib promotes selective and controlled proliferation of beta cells and improvement of beta cell function in ex vivo human islet cultures. Icovamenib enhances glycemic control in animal diabetic models. Icovamenib induces a dose-dependent enhancement in insulin secretion potentiated by the GLP-1 RA. Icovamenib can be used for the study of multiple hematologic malignancies, solid tumors, and diabetes mellitus, such as diffuse large B-cell lymphoma (DLBCL), multiple myeloma (MM) and chronic lymphocytic leukemia and type 2 diabetes [1] .
Bcl-2/Mcl-1-IN-4 (compound 20) is a dual inhibitor targeting Bcl-2 (Ki=0.49 μM) and Mcl-1 (Ki=0.51 μM). Bcl-2/Mcl-1-IN-4 significantly inhibits cancer cell proliferation and effectively induces apoptosis in U937 cells. Bcl-2/Mcl-1-IN-4 can be used in cancer research [1].
A-1210477 is a potent and selective inhibitor of MCL-1 with a Ki of 0.45 nM [1]. A-1210477 specifically binds MCL-1 and promotes apoptosis of cancer cells in an MCL-1-dependent manner .
UMI-77 is a selective Mcl-1inhibitor, which shows high binding affinity to Mcl-1 (IC50=0.31 μM). UMI-77 binds to the BH3 binding groove of Mcl-1 with Ki of 490 nM, showing selectivity over other members of anti-apoptotic Bcl-2 members.
A-1248767 is a MCL-1inhibitor (IC50=23.9 nM; Ki=0.41 nM) with anticancer activity. A-1248767, a derivative of A-1210477 (HY-12468), binds to MCL-1 with high affinity, induces the increase of intracellular MCL-1 protein, and promotes tumor cell apoptosis[1].
UMI-77-d4 is the deuterium labeled UMI-77. UMI-77 is a selective Mcl-1inhibitor, which shows high binding affinity to Mcl-1 (IC50=0.31 μM). UMI-77 binds to the BH3 binding groove of Mcl-1 with Ki of 490 nM, showing selectivity over other members of anti-apoptotic Bcl-2 members.
GQN-B37-E is a potent selective binder and inhibitor of MCL-1. GQN-B37-E binds to the BH3-domain-binding pocket in MCL-1. GQN-B37-E exhibits binding affinity for MCL-1 at the submicromolar range (Ki = 0.6 μM) without apparent binding to BCL-2 or BCL-XL [1].
M24 is a Mcl-1 selective inhibitor. M24 exhibits good binding affinity against Mcl-1 with Ki value of 0.33 μM. M24 exhibits good anti-proliferative activity and induce apoptosis in HepG2 cells [1].
BRD-810 is a highly selective MCL1inhibitor. BRD-810 can bind to the BH3 groove of MCL1 and block the sequestration of pro-apoptotic proteins, quickly inducing caspase activation in MCL1-dependent cell lines. BRD-810 shows anti-tumor activity in models of blood cancers and solid tumors [1].
dMCL1-2 is a potent and selective PROTAC of myeloid cell leukemia 1(MCL1) (Bcl-2 family member) based on Cereblon, which binds to MCL1 with a KD of 30 nM. dMCL1-2 activats the cellular apoptosis machinery by degradation of MCL1[1].
A-1155905 is a MCL-1inhibitor (IC50=33.5 nM; Ki=0.58 nM) with anticancer activity. A-1155905 selectively binds to MCL-1 with sufficient affinity to disrupt the MCL-1-bim complex in living cells. A-1155905-induced death of MCL-1-dependent cell lines is caspase-dependent and occurs via apoptosis[1].
Voruciclib is an orally active and selective CDKinhibitor with Ki values of 0.626 nM-9.1 nM. Voruciclib potently blocks CDK9, the transcriptional regulator of MCL-1. Voruciclib represses expression of MCL-1 in multiple models of diffuse large B-cell lymphoma (DLBCL) [1].
Voruciclib hydrochloride is an orally active and selective CDKinhibitor with Ki values of 0.626 nM-9.1 nM. Voruciclib hydrochloride potently blocks CDK9, the transcriptional regulator of MCL-1. Voruciclib hydrochloride represses expression of MCL-1 in multiple models of diffuse large B-cell lymphoma (DLBCL) [1].
Murizatoclax (AMG 397) is a potent, selective and orally active inhibitor of myeloid leukemia 1(MCL-1)inhibitor, with a Ki of 15 pM. Murizatoclax competitive binds to the BH3-binding groove of MCL1 with pro-apoptotic BCL-2 family members. Murizatoclax can be used for the research of cancer [1] .
(S,R)-S63845 is the isomer of S63845 (HY-100741), and can be used as an experimental control. S63845 is a potent and selective myeloid cell leukemia 1(MCL1)inhibitor with a Kd of 0.19 nM for human MCL1[1].
(R,R)-S63845 is the isomer of S63845 (HY-100741), and can be used as an experimental control. S63845 is a potent and selective myeloid cell leukemia 1(MCL1)inhibitor with a Kd of 0.19 nM for human MCL1[1].
AZD-5991 is a potent and selective Mcl-1inhibitor with an IC50 of 0.7 nM in FRET assay and a Kd of 0.17 nM in surface plasmon resonance (SPR) assay [1].
TC11 is a MCL1 degrader and Caspase-9 and CDK1 activator. TC11 functions as a phenylacetylamide derivative and is structurally related to immunomodulatory active molecules. TC11 induces degradation of MCL1 leading to apoptotic death [1] during prolonged mitotic arrest.
Maritoclax (Marinopyrrole A) is a novel and specific Mcl-1inhibitor with an IC50 value of 10.1 μM, and shows >8 fold selectivity than BCL-xl (IC50 > 80 μM).
(-)BI97D6 is a broad-spectrum inhibitor of the Bcl-2 protein family, inhibitingMcl-1, Bcl-2, Bcl-xL and Bcl-1 with IC50 values of 0.025, 0.031, 0.076 and 0.122 μM, respectively. (-)BI97D6 stimulates cell death through the Bak and Bax mediated mitochondrial apoptosis pathway. In addition, (-)BI97D6 inhibitsMcl-1 and can effectively induce apoptosis in acute myeloid leukemia (AML) cells [1].
NSC260594 induces Apoptosis. NSC260594 binds the shallow groove of the Mcl-1 protein, and inhibitsMcl-1 expression through down-regulation of Wnt signaling proteins. NSC260594 can also recognize G9-G10-A11-G12 RNA tetraloop of HIV and prevent the binding of the Gag protein within the 5’-UTR. NSC260594 inhibits tumor growth, and can be used for research of Triple-negative breast cancers (TNBCs) [1].
AZD-5991 S-enantiomer is the less active enantiomer of AZD-5991. AZD-5991 S-enantiomer is a Mcl-1inhibitor with an IC50 of 6.3 μM in FRET assay and a Kd of 0.98 μM in surface plasmon resonance (SPR) assay.
ABBV-467 is a selective MCL-1inhibitor (Ki: <0.01 nM). ABBV-467 induces apoptosis. ABBV-467 induces cancer cell death and inhibits tumor growth in models of hematological malignancies, such as multiple myeloma [1].
(R)-(-)-Gossypol (AT-101) is the levorotatory isomer of a natural product Gossypol. AT-101 is determined to bind to Bcl-2, Mcl-1 and Bcl-xL proteins with Kis of 260±30 nM, 170±10 nM, and 480±40 nM, respectively.
Maritoclax (Standard) is the analytical standard of Maritoclax. This product is intended for research and analytical applications. Maritoclax (Marinopyrrole A) is a novel and specific Mcl-1inhibitor with an IC50 value of 10.1 μM, and shows >8 fold selectivity than BCL-xl (IC50 > 80 μM).
PBX-7011 TFA is a derivative of camptothecin (HY-16560), which inhibits expressions of the cancer related survival genes DDX5, Survivin, Mcl-1 and XIAP in cells FaDu, degrades DDX5 proteins and exhibits anticancer activity [1].
TM-233 is an inhibitor of the JAK/STAT and NF-κB signaling pathways, exhibiting significant antitumor activity. TM-233 reduces the expression of the anti-apoptotic protein Mcl-1 by inhibiting the phosphorylation of JAK2 and STAT3, and regulates its transcription by directly binding to the Mcl-1 gene promoter. Additionally, TM-233 prevents the translocation of NF-κB from the cytoplasm to the nucleus by inhibiting its DNA-binding activity, thereby reducing nuclear NF-κB expression. TM-233 shows potential in overcoming Bortezomib (HY-10227) resistance and can be applied in research related to multiple myeloma [1].
SC-2001 is a compound structurally related to obatoclax that has better antitumor effects than obatoclax in liver cancer cell lines, downregulating Mcl-1 protein levels, inhibiting STAT3 phosphorylation, inducing apoptosis, and enhancing SHP1 expression and activity.
(E/Z)-CU-3 is a MCL-1 modulator. (E/Z)-CU-3 can be used to study hyperproliferative diseases, angiogenic diseases, cell cycle regulation diseases, autophagy regulation diseases, inflammatory diseases and/or infectious diseases [1].
(R)-(-)-Gossypol acetic acid (AT-101 (acetic acid)) is the levorotatory isomer of a natural product Gossypol. AT-101 is determined to bind to Bcl-2, Mcl-1 and Bcl-xL proteins with Kis of 260±30 nM, 170±10 nM, and 480±40 nM, respectively.
NoxaBH3 is a cysteine-based cross-linked peptide with increased cell permeability and higher inhibitory activity against Mcl-1. NoxaBH3 binds to the endogenous CXCR4 ligand to produce ubiquitin-Noxabh3 conjugate. NoxaBH3 is then delivered to cancer cells [1].
NH2-C6-NH-Boc is a PROTAC linker which refers to the alkyl/ether composition. NH2-C6-NH-Boc can be used in the synthesis the Mcl-1inhibitor based on PROTAC [1].
A-1208746 is an inhibitor for MCL-1, with a Ki of 0.454 nM. A-1208746 activates caspase-3/-7, induces apoptosis in cell H929, and decreases mitochondrial membrane potential. A-1208746 synergies with Navitoclax (HY-10087), and can be used in cancer research [1].
PROTAC Bcl2 degrader-1 (Compound C5) is a PROTAC based on Cereblon ligand, which potently and selectively induces the degradation of Bcl-2 (IC50, 4.94 μM; DC50, 3.0 μM) and Mcl-1 (IC50, 11.81 μM) by introducing the E3 ligase cereblon (CRBN)-binding ligand pomalidomide to Mcl-1/Bcl-2 dual inhibitorNap-1[1] (Blue: CRBN ligand, Black: linker;Pink: Mcl-1/Bcl-2 inhibitor, Nap-1).
CDK9-IN-24 (compound 21a) is a highly selective CDK9inhibitor with significant inhibitory effect on tumor growth. CDK9-IN-24 effectively blocks cell proliferation and induces apoptosis by downregulating Mcl-1 and c-Myc, and can be used in acute myeloid leukemia research [1].
Apogossypolone (ApoG2) is an orally active Bcl-2 family proteinsinhibitor with Ki values of 35, 25 and 660 nM for Bcl-2, Mcl-1 and Bcl-XL, respectively. Apogossypolone shows antitumor activities, induces cell apoptosis[1] and autophagy . Apogossypolone also has antifungal activity .
YX0798 is a selective and orally active CDK9inhibitor (Kd: 0.28 nM). YX0798 downregulates the oncoprotein c-MYC and pro-survival protein MCL-1. YX0798 disrupts the cell cycle and results in transcriptomic reprogramming, eventually leading to cell apoptosis. YX0798 has antitumor activity [1].
YCW-E11 is a Bcl-2, and Mcl-1inhibitor with Ki values of 0.83 and 0.33 μM, respectively. YCW-E11 induces cell apoptosis through the mitochondrial pathway and exhibits antitumor activity. YCW-E11 can be utilized in cancer research [1].
BH3 hydrochloride, a BBB penetrated peptide, provoke apoptosis either by direct activation of pro-apoptotic Bax/Bak or by neutralizing anti-apoptotic Bcl-2 proteins (Bcl-2, Bcl-XL, Bcl-w, Mcl-1 and A-1) via their BH3 domian [1] .
Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression [1]. Jaceosidin exhibits anti-cancer , anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation .
AZ-PFKFB3-67 is a potent and selective PFKFB3 kinase inhibitor with IC50s of 11, 159 and 1130 nM for PFKFB3, PFKFB2 and PFKFB1, respectively. AZ-PFKFB3-67 reduces MCL-1. AZ-PFKFB3-67 has neuroprotective activity [1] .
Sabutoclax is a potent and effective Bcl-2 Family (Bcl-2, Bcl-XL, Mcl-1, Bfl-1) inhibitor with IC50s of 0.32 μM, 0.31 μM, 0.20 μM, and 0.62 μM, respectively. Sabutoclax increases Bax, Bim, PUMA and survivin expression [1] .
MLS-0053105, a chloromaleimide, is a selective BFL-1inhibitor with an IC50 of 0.4 µM for Bfl-1/F-Bid. MLS-0053105 shows over 10 times less potent inhibition of Bcl-W, Bcl-2, and Bcl-XL and no activity against Bcl-B and Mcl-1[1].
Unesbulin (PTC596) is an orally active and selective B-cell-specific Moloney murine leukemia virus integration site 1(BMI-1)inhibitor. Unesbulin downregulates MCL-1 and induces p53-independent mitochondrial apoptosis in acute myeloid leukemia (AML) cells. Unesbulin has anti-leukemic activity [1] .
SACLAC, a Ceramide analog, is a potent and covalent acid ceramidase (ASAH1; AC)inhibitor with a Ki of 97.1 nM. SACLAC effectively blocks AC activity and induces a decrease in sphingosine 1-phosphate (S1P) and total ceramide levels. SACLAC reduces the levels of splicing factor SF3B1 and alternative Mcl-1 mRNA splicing, increases pro-apoptotic Mcl-1S levels to induce apoptosis in acute myeloid leukemia (AML) cells. SACLAC reduces the leukemic burden in human AML xenograft mouse models [1] .
Clitocine, an adenosine nucleoside analog isolated from mushroom, is a potent and efficacious readthrough agent. Clitocine acts as a suppressor of nonsense mutations and can induce the production of p53 protein in cells harboring p53 nonsense-mutated alleles. Clitocine can induce apoptosis in multidrug-resistant human cancer cells by targeting Mcl-1. Anticancer activity [1] .
BT2 is a BCKDC kinase (BDK)inhibitor with an IC50 of 3.19 μM. BT2 binding to BDK triggers helix movements in the N-terminal domain, resulting in the dissociation of BDK from the branched-chain α-ketoacid dehydrogenase complex (BCKDC) [1]. BT2 (compound 4) is also a potent and selective Mcl-1inhibitor with a Ki value of 59 μM .
S65487 (VOB560), a potent and selective BCL-2inhibitor, is a proagent of S55746. S65487 is also active on BCL-2 mutations, such as G101V and D103Y. S65487 has poor affinity with MCL-1, BFL-1 and BCL-XL. S65487 induces apoptosis and has anticaner activities [1] .
S65487 (VOB560) hydrochloride, a potent and selective Bcl-2inhibitor, is a proagent of S55746. S65487 hydrochloride is also active on BCL-2 mutations, such as G101V and D103Y. S65487 hydrochloride has poor affinity with MCL-1, BFL-1 and BCL-XL. S65487 hydrochloride induces apoptosis and has anticaner activities [1] .
CP-07 is a potent and selective PROTACCDK9 degrader (DC50: 43 nM). CP-07 inhibits 22RV1 cell proliferation (IC50: 62 nM) and colony formation by down-regulating Mcl-1 and c-Myc. CP-07 inhibits 22RV1 xenograft tumor growth. CP-07 can be used for research of prostate cancer [1].
Jaceosidin (Standard) is the analytical standard of Jaceosidin. This product is intended for research and analytical applications. Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression [1]. Jaceosidin exhibits anti-cancer , anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation .
RMS5, a tetrandrine analogue, is a potent P-glycoprotein (P-gp)inhibitor. RMS5 has markedly antiproliferative and cytotoxic effects on cancer cells. RMS5 slightly diminishes the expression of the anti-apoptotic Bcl-2 family proteins Bcl-XL and Mcl-1. RMS3 causes PARP cleavage, a marker for cells undergoing apoptosis. RMS5 has strong anticancer property [1].
Gambogic Acid (Beta-Guttiferrin) is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic Acid (Beta-Guttiferrin) inhibitsBcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50s of 1.47 μM, 1.21 μM, 2.02 μM, 0.66 μM, 1.06 μM and 0.79 μM.
S65487 (VOB560) sulfate, a potent and selective Bcl-2inhibitor, is a proagent of S55746. S65487 sulfate is also active on BCL-2 mutations, such as G101V and D103Y. S65487 sulfate has poor affinity with MCL-1, BFL-1 and BCL-XL. S65487 sulfate induces apoptosis and has anticaner activities [1] .
rel-AZ5576 is a selective CDK9 inhibitor with the activity of downregulating Mcl-1 and MYC mRNA transcription and protein expression in diffuse large B-cell lymphoma by inhibiting CDK9, promoting MYC protein turnover, reducing MYC phosphorylation on the stable Ser62 residue and downregulating MYC transcriptional targets, inhibiting the growth of diffuse large B-cell lymphoma cell lines in vitro and in vivo and independent of the cell origin.
BAY 61-3606 hydrochloride is an orally available, ATP-competitive, reversible and highly selective Syk inhibitor with a Ki of 7.5 nM and an IC50 of 10 nM . BAY 61-3606 hydrochloride reduces ERK1/2 and Akt phosphorylation in neuroblastoma cell. BAY 61-3606 hydrochloride induces a large decrease of Syk phosphorylation in K-rn cell lysates. BAY 61-3606 hydrochloride sensitizes TRAIL-induced apoptosis by downregulating Mcl-1 in breast cancer cells.
GQN-B37-Me is a MCL-1inhibitor. GQN-B37-Me induces caspase-dependent apoptosis. GQN-B37-Me exhibits noteworthy cytotoxicity in H929 (IC50 = 3.71 μM) and MV-4-11 (IC50 = 5.57 μM) cells. GQN-B37-Me can be used for the research of leukemia [1].
BAY 61-3606 is an orally available, ATP-competitive, reversible and highly selective Sykinhibitor with a Ki of 7.5 nM and an IC50 of 10 nM [1]. BAY 61-3606 reduces ERK1/2 and Akt phosphorylation in neuroblastoma cell . BAY 61-3606 induces a large decrease of Syk phosphorylation in K-rn cell lysates . Bay 61-3606 sensitizes TRAIL-induced apoptosis by downregulating Mcl-1 in breast cancer cells .
Zotiraciclib hydrochloride is a novel small molecule multi-target enzyme inhibitor with activity in inhibiting tumor growth. Zotiraciclib hydrochloride exerts its anti-tumor effect by reducing the level of Myc through inhibiting cyclin-dependent kinase 9 (CDK9). Zotiraciclib hydrochloride may be useful for inhibiting cancers that cross the blood-brain barrier. The high protein level of MCL-1 of Zotiraciclib hydrochloride is associated with survival, suggesting that it may serve as a prognostic factor and inhibitory target in further studies [1].
BAY 61-3606 dihydrochloride is an orally available, ATP-competitive, reversible and highly selective Sykinhibitor with a Ki of 7.5 nM an IC50 of 10 nM [1]. BAY 61-3606 dihydrochloride reduces ERK1/2 and Akt phosphorylation in neuroblastoma cell . BAY 61-3606 dihydrochloride induces a large decrease of Syk phosphorylation in K-rn cell lysates . Bay 61-3606 dihydrochloride sensitizes TRAIL-induced apoptosis by downregulating Mcl-1 in breast cancer cells .
CDK9-IN-36 (Compound T7) is a potent, selective and metabolically stable CDK9inhibitor with an IC50 value of 1.2 nM. CDK9-IN-36 effectively suppresses cell proliferation, reduces colony formation, and induces apoptosis in Osimertinib (HY-15772)-resistant NSCLC cells by downregulating Mcl-1. CDK9-IN-36 also demonstrates antitumor efficacy in a tumor xenograft model [1].
STAT3-IN-38 (Compound 4m) is an inhibitor of STAT3 (KD of rhSTAT3: 45.33 µM). STAT3-IN-38 binds to the SH2 domain of STAT3 protein and suppresses the STAT3’s phosphorylation at site pTyr705 as well as its downstream genes (Survivin and Mcl-1). STAT3-IN-38 could block cell-cycle and induce Apoptosis in colorectal cancer cells [1].
IMB-XH1 is an inhibitor of myeloid cell factor 1(Mcl-1)[1]. IMB-XH1 is a non-competitive Delhi metallo-β-lactamase(NDM-1)inhibitor. The IC50s of IMB-XH1 against metallo-β-lactamases NDM-1, IMP-4, ImiS and L1 are 0.4637 μM, 3.980 μM, 0.2287 μM and 1.158 μM, respectively .
CMLD010509 (SDS-1-021) is a highly specific inhibitor of the oncogenic translation program supporting multiple myeloma (MM)-including key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1. CMLD010509 (SDS-1-021) shows an IC50 below 10 nM for most MM cell lines and induces apoptosis. CMLD010509 (SDS-1-021) is a potent and selective translation inhibitor through an eIF4E phosphorylation-independent mechanism [1].
Gambogic Acid (Standard) is the analytical standard of Gambogic Acid. This product is intended for research and analytical applications. Gambogic Acid (Beta-Guttiferrin) is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic Acid (Beta-Guttiferrin) inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50s of 1.47 μM, 1.21 μM, 2.02 μM, 0.66 μM, 1.06 μM and 0.79 μM.
STAT3-IN-11 (7a) is a selective STAT3inhibitor that inhibits the phosphorylation of STAT3 at site pTyr705. STAT3-IN-11 inhibits the phosphorylation of downstream genes (Survivin and Mcl-1) without affecting its upstream tyrosine kinases (Src and JAK2) levels and p-STAT1 expression. STAT3-IN-11 can induce cancer cell apoptosis, which is potential for the discovery of effective STAT3 inhibitors and antitumor agents against cancers [1].
Ch282-5 is an orally active inhibitor targeting the Bcl-2 protein, inducing mitochondria-dependent apoptosis (Apoptosis) by disrupting mitophagy and the mTOR pathway. Ch282-5 exhibits antiproliferative activity against colorectal cancer cells both in vitro and in vivo, and it also inhibits metastasis. Additionally, Ch282-5 enhances Oxaliplatin (HY-17371)-induced autophagy (Autophagy) by downregulating the Mcl-1 protein and increasing platelet count, alleviating adverse effects of Navitoclax (HY-10087) [1].
AZD1897 is a PIM1, PIM2, and PIM3inhibitor with IC50 values of less than 3 nM for these three PIM kinases. AZD1897 exhibits anticancer activity and synergistically inhibits the activity of acute myeloid leukemia (AML) cells in combination with Capivasertib (HY-15431). This synergistic inhibitory effect is achieved through the inhibition of the mTOR and MCL1 pathways [1] .
(-)-CMLD010509 ((-)-SDS-1-021) is an isomer of CMLD010509 (SDS-1-021) (HY-119271). CMLD010509 (SDS-1-021) is a highly specific inhibitor of the oncogenic translation program supporting multiple myeloma (MM)-including key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1. CMLD010509 (SDS-1-021) shows an IC50 below 10 nM for most MM cell lines and induces apoptosis. CMLD010509 (SDS-1-021) is a potent and selective translation inhibitor through an eIF4E phosphorylation-independent mechanism [1].
Angelicin is a furanocoumarin compound that functions as an inhibitor of NF-κB and MAPK signaling pathways, exhibiting anti-inflammatory, antiviral, and antitumor activities. It suppresses the lytic replication of γ-herpesviruses, such as MHV-68, early during viral infection, potentially inhibitingRTA gene expression (IC50=28.95 μM). Angelicin also mitigates inflammation by inhibiting the phosphorylation and nuclear translocation of NF-κB, and the phosphorylation of p38 and JNK. Furthermore, it induces apoptosis in neuroblastoma cells by downregulating anti-apoptotic proteins like Bcl-2, Bcl-xL, and Mcl-1, while activating caspase-9 and caspase-3.
P1D-34 is a Pin1PROTAC degrader with a DC50 value of 177 nM. P1D-34 also down-regulates Pin1 client proteins such as Cyclin D1, Rb, Mcl-1, Akt, and c-Myc. P1D-34 shows anti-proliferative activities in a panel of acute myeloid leukemia (AML) cell lines. P1D-34 induces cell DNA damage and apoptosis by releasing ROS generation. Pink: PIN1 ligand (HY-171442A), Blue: CRBN ligand (HY-14658), Black: Linker (HY-W014883) [1].
CDKI-83 is a potent CDK9 and CDK1inhibitor with Ki values of 21 nM and 72 nM for CDK9/T1 and CDK1/B, respectively. CDKI-83 demonstrates effective anti-proliferative activity in human tumour cell lines with a GI50<1 μM. CDKI-83 effectively induces apoptosis in A2780 human ovarian cancer cells. CDKI-83 reduces phosphorylation at Ser-2 of RNA polymerase II (RNAPII) by inhibiting cellular CDK9 activity, and down-regulates Mcl-1 and Bcl-2. CDKI-83 has the potential for anti-cancer research [1].
Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe [1] .
(S)-Sabutoclax ((S)-BI-97C1), an optically pure apogossypol derivative, is pan-active inhibitor of antiapoptotic B-cell lymphoma/leukemia-2 (Bcl-2) family proteins. (S)-Sabutoclax (Compound II) inhibits the binding of BH3 peptides to Bcl-XL, Bcl-2, Mcl-1, and Bfl-1 with IC50 values of 0.31, 0.32, 0.20, and 0.62 μM, respectively. (S)-Sabutoclax also potently inhibits cell growth of human prostate cancer, lung cancer, and lymphoma cell lines with EC50 values of 0.13, 0.56, and 0.049 μM, respectively. (S)-Sabutoclax can be used for the research of apoptosis-based therapies against cancer [1].
CDK9-IN-33 (compound C35) is a potent, selective and orally active CDK9inhibitor with IC50 values of 17.44, 160, 316.30, 1771.00, >10000 nM for CDK9, CDK7, CDK2, CDK4, CDK6 respectively. CDK9-IN-33 induces apoptosis. CDK9-IN-33 decreases the protein expression of RPB1 CTD Ser2, RPB1, MCL1. CDK9-IN-33 shows anti-tumor activity [1].
Chromomycin A3 (Standard) is the analytical standard of Chromomycin A3 (HY-W040129). This product is intended for research and analytical applications. Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe [1] .
Bruceantinol is a quassinoid that can be isolated from Brucea javanica, inhibitspepper mottle virus (PepMoV) in pepper. Bruceantinol is a STAT3inhibitor demonstrating potent antitumor activity in in vitro and in vivo human colorectal cancer (CRC) models. Bruceantinol has potent anti-leukemic activity. Bruceantinol strongly inhibits STAT3 DNA-binding ability (IC50 = 2.4 pM), blocks the constitutive and IL-6-induced STAT3 activation, and suppresses transcription of MCL-1, PTTG1, survivin and c-Myc. Bruceantinol binds with CDK2/4/6 to facilitate protein degradation through proteasome pathway. Bruceantinol can dose- and time-dependently reduces the cell growth, impede cell proliferation, disrupts the cell cycle, and induces necrosis in MCF-7 cells and apoptosis in MDA-MB-231 cells [1] .
(+)-Enitociclib ((+)-BAY-1251152) is the enantiomer of Enitociclib (HY-103019E) with (+) optical rotation. Enitociclib is a selective CDK9inhibitor and apoptosis inducer. Enitociclib inhibits CDK9 activity and reduces the phosphorylation of Ser2 in the carboxyl-terminal domain (CTD) of RNA polymerase Pol II, thereby downregulating the transcription of key oncogenes such as MYC and MCL1. Enitociclib has anti-proliferative activity targeting MYC + lymphoma and multiple myeloma (MM) cells, and has synergistic effects with Bortezomib (HY-10227) and Lenalidomide (HY-A0003), and can be used in the research of hematological malignancies [1] .
(±)-Enitociclib ((±)-BAY-1251152) is the racemic mixture of Enitociclib (HY-103019E). Enitociclib is a selective CDK9inhibitor and apoptosis inducer. Enitociclib inhibits CDK9 activity and reduces the phosphorylation of Ser2 in the carboxyl-terminal domain (CTD) of RNA polymerase Pol II, thereby downregulating the transcription of key oncogenes such as MYC and MCL1. Enitociclib has anti-proliferative activity targeting MYC + lymphoma and multiple myeloma (MM) cells, and has synergistic effects with Bortezomib (HY-10227) and Lenalidomide (HY-A0003), and can be used in the research of hematological malignancies [1] .
(-)-Enitociclib ((R)-Enitociclib) is an enantiomer of Enitociclib (HY-103019E) with an optical rotation of (-). Enitociclib is a selective CDK9inhibitor and apoptosis inducer. Enitociclib inhibits CDK9 activity and reduces the phosphorylation of Ser2 in the carboxyl-terminal domain (CTD) of RNA polymerase Pol II, thereby downregulating the transcription of key oncogenes such as MYC and MCL1. Enitociclib has anti-proliferative activity targeting MYC + lymphoma and multiple myeloma (MM) cells, and has synergistic effects with Bortezomib (HY-10227) and Lenalidomide (HY-A0003), and can be used in the research of hematological malignancies [1] .
CLZ-8 (Compound 8) is an orally active Mcl-1-PUMA interface inhibitor, with a Ki of 0.3 μM. CLZ-8 exhibits dual activity on reduce PUMA-dependent apoptosis while deactivating Mcl-1-mediated anti-apoptosis in cancer cells [1].
GBD-9 is a degrader based on the E3 ubiquitin ligase CRBN that targets BTK and the G1 to S phase transition protein GSPT1. GBD-9 has both PROTAC and molecular glue properties by inducing ubiquitination and proteasomal degradation of target proteins. GBD-9 can efficiently degrade wild-type and mutant BTK (such as C481S mutation) and GSPT1. GBD-9 significantly inhibits tumor cell proliferation by inducing G1 phase arrest in cancer cells, downregulating anti-apoptotic proteins (BCL-2, MCL-1) and activating Caspase-3 to induce apoptosis. GBD-9 is mainly used in the research of hematological tumors such as diffuse large B-cell lymphoma (DLBCL) and acute myeloid leukemia (AML) [1] .
GBD-9 is composed of E3 ubiquitin ligase ligand (pink part) 5-Aminothalidomide (HY-W023573), target protein ligand (blue part) Btk Inhibitor: IBT6A (HY-13036A), and PROTAC linker (black part) Nonanoic acid (HY-N7057).
(rac)-ZK-304709 is an isoform of ZK-304709 and is an orally active multi-targeted tumor growth inhibitor that inhibits multiple cell cycle-dependent kinases (CDKs), vascular endothelial growth factor receptor kinases (VEGF-RTKs), and platelet-derived growth factor receptor kinase β (PDGF-RTKβ). (rac)-ZK-304709 can dose-dependently inhibit the proliferation and colony formation of neuroendocrine tumor (NET) cells. (rac)-ZK-304709 directly acts on NET cells by inducing G2 cell cycle arrest and apoptosis, while reducing the expression of MCL1, survivin, and HIF1α. (rac)-ZK-304709 effectively controls tumor growth by inducing apoptosis and inhibiting tumor-induced angiogenesis, and may become a potential agent for inhibiting NET [1].
HS-291 is a HtpGinhibitor of Borrelia burgdorferi (Bb). HS-291 contains BX-2819 (high affinity for Bb HtpG), PEG linker, and Verteporfin (HY-B0146) (a photoactive toxin).HS-291 produces reactive oxygen species under light activation to oxidize HtpG and a discrete protein subset near chaperone proteins and can quickly and irreversibly inactivate Bb [1].
Furowanin A is a flavonoid with anti-neoplastic effects. Furowanin A inhibitsSTAT3/Mcl-1 axis to suppress proliferation, block cell cycle progression, induce apoptosis and promote autophagy. Furowanin A potently inhibits colorectal cancer (CRC) cells [1].
LP-284 is a potent DNA alkylating agent that kills solid tumours. LP-284 can be used in the studies of hematologic cancers with compromised DNA repair, such as mantle cell lymphoma (MCL) .
Topoisomerase I inhibitor 21 (Compound 3e) is an inhibitor for Topoisomerase I through stabilization of enzyme-DNA complex. Topoisomerase I inhibitor 21 exhibits antiproliferative activity in 39 human cancer cells (JFCR39) with mean GI50 39 nM [1].
BI-1206 is a recombinant and antagonistic human monoclonal antibody targeting FcγRIIB (CD32B). BI-1206 can block CD20 internalization induced by Rituximab (HY-P9913) itself or combined with others including Ibrutinib (HY-10997), Venetoclax (HY-15531), and CHOP. BI-1206 can enhance or recover the activity of Rituximab or other anti-CD20 monoclonal antibodies. BI-1206 has cytolytic activity against malignant B cells. BI-1206 can be studied for cancer research such as mantle cell lymphoma (MCL) .
BH3 hydrochloride, a BBB penetrated peptide, provoke apoptosis either by direct activation of pro-apoptotic Bax/Bak or by neutralizing anti-apoptotic Bcl-2 proteins (Bcl-2, Bcl-XL, Bcl-w, Mcl-1 and A-1) via their BH3 domian [1] .
P-gp inhibitor 21 (Compound 56) is an inhibitor for P-glycoprotein (P-gp) transport, which reverses P-gp-mediated multidrug resistance (MDR) and exhibits antitumor efficacy in mice without significant cytotoxicity [1].
NoxaBH3 is a cysteine-based cross-linked peptide with increased cell permeability and higher inhibitory activity against Mcl-1. NoxaBH3 binds to the endogenous CXCR4 ligand to produce ubiquitin-Noxabh3 conjugate. NoxaBH3 is then delivered to cancer cells [1].
BI-1206 is a recombinant and antagonistic human monoclonal antibody targeting FcγRIIB (CD32B). BI-1206 can block CD20 internalization induced by Rituximab (HY-P9913) itself or combined with others including Ibrutinib (HY-10997), Venetoclax (HY-15531), and CHOP. BI-1206 can enhance or recover the activity of Rituximab or other anti-CD20 monoclonal antibodies. BI-1206 has cytolytic activity against malignant B cells. BI-1206 can be studied for cancer research such as mantle cell lymphoma (MCL) .
(R)-(-)-Gossypol (AT-101) is the levorotatory isomer of a natural product Gossypol. AT-101 is determined to bind to Bcl-2, Mcl-1 and Bcl-xL proteins with Kis of 260±30 nM, 170±10 nM, and 480±40 nM, respectively.
Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression [1]. Jaceosidin exhibits anti-cancer , anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation .
Clitocine, an adenosine nucleoside analog isolated from mushroom, is a potent and efficacious readthrough agent. Clitocine acts as a suppressor of nonsense mutations and can induce the production of p53 protein in cells harboring p53 nonsense-mutated alleles. Clitocine can induce apoptosis in multidrug-resistant human cancer cells by targeting Mcl-1. Anticancer activity [1] .
Gambogic Acid (Beta-Guttiferrin) is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic Acid (Beta-Guttiferrin) inhibitsBcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50s of 1.47 μM, 1.21 μM, 2.02 μM, 0.66 μM, 1.06 μM and 0.79 μM.
Angelicin is a furanocoumarin compound that functions as an inhibitor of NF-κB and MAPK signaling pathways, exhibiting anti-inflammatory, antiviral, and antitumor activities. It suppresses the lytic replication of γ-herpesviruses, such as MHV-68, early during viral infection, potentially inhibitingRTA gene expression (IC50=28.95 μM). Angelicin also mitigates inflammation by inhibiting the phosphorylation and nuclear translocation of NF-κB, and the phosphorylation of p38 and JNK. Furthermore, it induces apoptosis in neuroblastoma cells by downregulating anti-apoptotic proteins like Bcl-2, Bcl-xL, and Mcl-1, while activating caspase-9 and caspase-3.
Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe [1] .
Bruceantinol is a quassinoid that can be isolated from Brucea javanica, inhibitspepper mottle virus (PepMoV) in pepper. Bruceantinol is a STAT3inhibitor demonstrating potent antitumor activity in in vitro and in vivo human colorectal cancer (CRC) models. Bruceantinol has potent anti-leukemic activity. Bruceantinol strongly inhibits STAT3 DNA-binding ability (IC50 = 2.4 pM), blocks the constitutive and IL-6-induced STAT3 activation, and suppresses transcription of MCL-1, PTTG1, survivin and c-Myc. Bruceantinol binds with CDK2/4/6 to facilitate protein degradation through proteasome pathway. Bruceantinol can dose- and time-dependently reduces the cell growth, impede cell proliferation, disrupts the cell cycle, and induces necrosis in MCF-7 cells and apoptosis in MDA-MB-231 cells [1] .
Jaceosidin (Standard) is the analytical standard of Jaceosidin. This product is intended for research and analytical applications. Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression [1]. Jaceosidin exhibits anti-cancer , anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation .
Gambogic Acid (Standard) is the analytical standard of Gambogic Acid. This product is intended for research and analytical applications. Gambogic Acid (Beta-Guttiferrin) is derived from the gamboges resin of the tree Garcinia hanburyi. Gambogic Acid (Beta-Guttiferrin) inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50s of 1.47 μM, 1.21 μM, 2.02 μM, 0.66 μM, 1.06 μM and 0.79 μM.
Chromomycin A3 (Standard) is the analytical standard of Chromomycin A3 (HY-W040129). This product is intended for research and analytical applications. Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe [1] .
Furowanin A is a flavonoid with anti-neoplastic effects. Furowanin A inhibitsSTAT3/Mcl-1 axis to suppress proliferation, block cell cycle progression, induce apoptosis and promote autophagy. Furowanin A potently inhibits colorectal cancer (CRC) cells [1].
NS3 protease Protein is a zinc-dependent serine protease.NS3 needs to bind to the viral protein NS4A to enable additional conformation changes that enhance activity and appropriate intracellular localization.NS3 protein induces Caspase-8-mediated apoptosis independently of its protease or helicase activity.NS3 protease Protein, HCV (GST) is the recombinant Virus-derived NS3 protease protein, expressed by E.coli , with N-GST labeled tag.
The VSTM2A protein is a key player in early white and brown preadipocyte differentiation and actively promotes adipogenesis by upregulating the transcription factor PPARG. This regulation operates in BMP4-dependent signaling pathways, highlighting the complex molecular mechanisms involved in differentiation. VSTM2A Protein, Human ( E84K, HEK293, His) is the recombinant human-derived VSTM2A protein, expressed by HEK293 , with C-6*His labeled tag and E84K mutation.
The hemagglutinin HA1 protein is essential for attachment of virions to host cells by binding to sialic acid-containing receptors, inducing virion internalization via clathrin-dependent or clathrin- and caveolin-independent pathways. As a class I viral fusion protein, HA1 determines host range restriction and virulence, mediating fusion between the virion membrane and the endosomal membrane. HA/Hemagglutinin Protein, H3N2 ( EPI189220, sf9, His) is the recombinant Virus-derived HA/Hemagglutinin protein, expressed by Sf9 insect cells , with C-His labeled tag.
UMI-77-d4 is the deuterium labeled UMI-77. UMI-77 is a selective Mcl-1inhibitor, which shows high binding affinity to Mcl-1 (IC50=0.31 μM). UMI-77 binds to the BH3 binding groove of Mcl-1 with Ki of 490 nM, showing selectivity over other members of anti-apoptotic Bcl-2 members.
MCL1 Antibody is a non-conjugated and Rabbit origined monoclonal antibody about 37 kDa, targeting to MCL1. It can be used for WB,ICC/IF,IHC-P,IP,FC assays with tag free, in the background of Human, Mouse.
MCL1 Antibod (YA4204) is a mouse-derived and non-conjugated IgG1 antibody, targeting to MCL-1. It can be applicated for WB, IHC-P, ICC/IF, ELISA assays, in the background of human.
Mcl1; BCL2L3; Induced myeloid leukemia cell differentiation protein Mcl-1; Bcl-2-like protein 3; Bcl2-L-3; Bcl-2-related protein EAT/Mcl1; Mcl1/EAT
WB, IHC-P, ICC/IF, ELISA
Human
MCL1 Antibod (YA4961) is a mouse-derived and non-conjugated monoclonal antibody, targeting to Mcl-1. It can be applicated for WB, IHC-P, ICC/IF, ELISA assays, in the background of human.
Mcl1; BCL2L3; Induced myeloid leukemia cell differentiation protein Mcl-1; Bcl-2-like protein 3; Bcl2-L-3; Bcl-2-related protein EAT/Mcl1; Mcl1/EAT
WB, IHC-P, ICC/IF, IP, ELISA
Human, Mouse, Rat
MCL1 Antibody (YA5869) is a rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to MCL1. It can be applicated for WB, IHC-P, ICC/IF, IP, ELISA assays, in the background of human, mouse, rat.
Mcl1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Mcl1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
MCL1 Human Pre-designed siRNA Set A contains three designed siRNAs for MCL1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Mcl1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Mcl1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
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