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DEL-22379 is an ERK dimerization Inhibitor. DEL-22379 readily binds to ERK2 with a Kd estimated in the low micromolar range, though binding is detectable even at low nanomolar concentrations. ERK2 dimerization is progressively inhibited with an IC50 of ~0.5 μM.
Mavelertinib is a selective, orally available and irreversible EGFR tyrosine kinase inhibitor (EGFR TKI), with IC50s of 5, 4, 12 and 3 nM for Del, L858R, and double mutants T790M/L858R and T790M/Del, respectively. Mavelertinib can be used for the research of non-small-cell lung cancer (NSCLC) .
CH7233163 is a noncovalent ATP-competitive inhibitor for EGFR-Del19/T790M/C797S. CH7233163 can overcome Osimertinib (HY-15772)-Resistant EGFR-Del19/T790M/C797S mutation. CH7233163 blocks the EGFR phosphorylation in the Del19/T790M/C797S_NIH3T3 cells. CH7233163 has antitumor activities .
KM11060 is a corrector of the F508 deletion (F508del)-cystic fibrosis transmembrane conductance regulator (CFTR) trafficking defect. KM11060 can be used for the research of F508del-CFTR processing defect and development of cystic fibrosis research .
Ivacaftor-d9 is a potent CFTR modulator and exhibits an EC50 value of 255 nM for CFTR potentiation in G551D/F508del HBE Cells. Ivacaftor-D9 acts as an orally active and improved deuterated Ivacaftor analog for cystic fibrosis research .
EGFR-IN-127 is an ATP-competitive EGFR inhibitor with IC50s of 136.3 nM and 161. 2 nM for EGFR del19 and EGFR del19/T790M/C797S, respectively. EGFR-IN-127 has the potential for the study of non-small-cell lung cancer (NSCLC) .
EGFR-IN-48 is a potent and orally active EGFR inhibitor with IC50s of 0.193 nM, 0.251 nM, 10.4 nM for EGFR d19/TM/CS, EGFR LR/TM/CS, EGFR WT, respectively. EGFR-IN-48 inhibits the proliferation of BaF3 EGFR del19/T790M/C797S and PC-9 EGFR del19/T790M/C797S cells with IC50s of 1.526, 66.7 nM, respectively .
EGFR-IN-27 is a potent EGFR inhibitor with IC50s of <50 nM for EGFR Del, L858R, Del/T790M, L858R/T790M, Del/T790M/C797S, and L858R/T790M/C797S, respectively (WO2021249324A1, compound 511) .
ARN23765 is a corrector for F508del-CFTR with an EC50 of 38 pM in human bronchial epithelial cells. ARN23765 improves the maturation and function of F508del-CFTR on the cell membrane, affects the ions transport and secretion, and corrects the pathological mechanism of cystic fibrosis (CF) .
EGFR-IN-89 (compound 13k) is a potent, fourth-generation EGFR mutation inhibitor with an IC50 of 10.1 nM against Del19/T790M/C797S mutations. EGFR-IN-89 shows higher selectivity over wild type .
Ivacaftor-d9 is a potent CFTR modulator and exhibits an EC50 value of 255 nM for CFTR potentiation in G551D/F508del HBE Cells. Ivacaftor-D9 acts as an orally active and improved deuterated Ivacaftor analog for cystic fibrosis research .
BI-4020 is a fourth-generation, orally active, and non-covalent EGFR tyrosine kinase inhibitor. BI-4020 inhibits not only the triple mutant EGFR del19 T790M C797S variant (IC50=0.2 nM in BaF3 cell lines) but also the double mutant EGFR del19 T790M and primary mutant EGFR del19 (IC50=1 nM). BI-4020 also shows activity against EGFR wt (IC50=190 nM). BI-4020 shows high kinome selectivity and good DMPK properties .
Tezacaftor (VX-661) is a F508del CFTR corrector. It helps CFTR protein reach the cell surface. However, Ivacaftor (VX-770, HY-13017), a CFTR potentiator, helps to prolong the opening time of cell surface CFTR protein channels. Tezacaftor combining with Ivacaftor, shows potent efficacy against cystic fibrosis and diseases with homozygous for the CFTR Phe508del mutation. Moreover, Elexacaftor (VX-445, HY-111772) is also a CFTR corrector. Elexacaftor-Tezacaftor-Ivacaftor aims at with cystic fibrosis (CF) with at least one Phe508del mutation, often avoids the indication for lung transplantation .
EGFR-IN-95 (compound 5j) is an 2,4-diaminonicotinamide derivative. EGFR-IN-95 has potent inhibitory activity against EGFRdel19/T790M/C797S and L858R/T790M/C797S .
EGFR-IN-98 (Compound 4c) is a EGFR inhibitor. The IC50 values of L858R/T790M/C797S and Del19/T790M/C797S are 0.277 μM and 0.089 μM, respectively. EGFR-IN 98 can be used in the study of tumors .
DS06652923 is an orally active EGFR triple mutation inhibitor. DS06652923 has a growth inhibition effect on Ba/F3 EGFR del19/T90M/C797S cells, with a GI50 value of 9.4 nM. DS06652923 can lead to tumor regression in Ba/F3 xenograft models .
EGFR-IN-104 (Compound A23) is an effective inhibitor of EGFR, with IC50 values of 0.33 μM and 0.133 μM against EGFR L858R/T790M and EGFR Del19/T790M/C797S, respectively. EGFR-IN-104 exhibits anticancer activity both in vitro and in vivo .
Tezacaftor (Standard) is the analytical standard of Tezacaftor. This product is intended for research and analytical applications. Tezacaftor (VX-661) is a F508del CFTR corrector. It helps CFTR protein reach the cell surface. However, Ivacaftor (VX-770, HY-13017), a CFTR potentiator, helps to prolong the opening time of cell surface CFTR protein channels. Tezacaftor combining with Ivacaftor, shows potent efficacy against cystic fibrosis and diseases with homozygous for the CFTR Phe508del mutation. Moreover, Elexacaftor (VX-445, HY-111772) is also a CFTR corrector. Elexacaftor-Tezacaftor-Ivacaftor aims at with cystic fibrosis (CF) with at least one Phe508del mutation, often avoids the indication for lung transplantation .
EGFR-TK-IN-1 (compound 7o) is a potent mutant EGFR inhibitor with IC50 of 8.5 nM an 9.3 nM against EGFR L858R/T790M and EGFR Del19.EGFR-TK-IN-1 showes strong antiproliferative effects against EGFR mutant-driven non-small cell lung cancer (NSCLC) cells and induces cell apoptosis .
ATX inhibitor 27 (Compound 31) is an ATX inhibitor. The IC50 values of ATX inhibitor 27 against human autotaxin (hATX) and lysophosphatidylcholine (LPC) are 13 nM and 23 nM, respectively. ATX inhibitor 27 reduces LPA levels in vivo by inhibiting ATX enzyme. ATX inhibitor 27 can be used in the study of ATX-LPA-related diseases such as inflammation, neurodegenerative diseases and cancer .
Tezacaftor-d6 (VX-661-d6) is deuterium labeled Tezacaftor. Tezacaftor (VX-661) is a F508del CFTR corrector. It helps CFTR protein reach the cell surface. However, Ivacaftor (VX-770, HY-13017), a CFTR potentiator, helps to prolong the opening time of cell surface CFTR protein channels. Tezacaftor combining with Ivacaftor, shows potent efficacy against cystic fibrosis and diseases with homozygous for the CFTR Phe508del mutation. Moreover, Elexacaftor (VX-445, HY-111772) is also a CFTR corrector. Elexacaftor-Tezacaftor-Ivacaftor aims at with cystic fibrosis (CF) with at least one Phe508del mutation, often avoids the indication for lung transplantation .
GLPG2451 is a cystic fibrosis transmembrane conductance regulator (CFTR) potentiator, which effectively potentiates low temperature rescued F508del CFTR with an EC50 of 11.1 nM .
RNF5 inhibitor inh-02 is a potent inhibitor of E3 ubiquitin ligase RNF5/RMA1. RNF5 inhibitor inh-02 leads to significant F508del-CFTR rescue (EC50=2.2 uM) in bronchial epithelial cells homozygous for the F508del mutation. RNF5 inhibitor inh-02 can be used for cystic fibrosis research .
EGFR kinase inhibitor 2 (compound A-7) is a potent EGFR inhibitor targeting EGFR L858R/T790M/C797S and EGFR Del19/T790M/C797S mutants. EGFR kinase inhibitor 2 has the potential to address acquired resistance in the treatment of non-small cell lung cancer .
EGFR-IN-140 (Compound 31) is the inhibitor for EGFR, that inhibits EGFR wildtype and EGFR L858R/T790M/C797S mutant with Ki of 0.95 nM and 2.1 nM, and inhibits EGFR del19/T790M/C797S in Ba/F3 with an IC50 of 56.9 nM. EGFR-IN-140 exhibits antitumor efficacy in mouse model .
(Rac)-Tezacaftor ((Rac)-VX-661) is a racemate of Tezacaftor (HY-15448). Tezacaftor is a F508del CFTR corrector. (Rac)-Tezacaftor can be used for the research of cystic fibrosis .
Navlimetostat hydrochloride is a potent first-in-class selective inhibitor of the PRMT5/MTA complex, with an IC50 of less than 10 nM in PRMT5/MTA MTAPDEL SDMA cells .
Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively.
EGFR mutant-IN-2 (Compound D51) is an EGFR mutant inhibitor. EGFR mutant-IN-2 inhibits the EGFR L858R/T790M/C797S mutant with an IC50 value of 14 nM. EGFR mutant-IN-2 inhibits the EGFR del19/T790M/C797S mutant with an IC50 value of 62 nM. EGFR mutant-IN-2 has favorable PK parameters, safety properties, in vivo stability, and antitumor activity .
Tezacaftor-d4 (VX-661-d4) is the deuterium-labeled Tezacaftor (HY-15448), a F508del CFTR corrector. Tezacaftor helps CFTR protein reach the cell surface .
Mutated EGFR-IN-2 (compound 91) is a mutant-selective EGFR inhibitor extracted from patent WO2017036263A1, which potently inhibits single-mutant EGFR (T790M) and double-mutant EGFR (including L858R/T790M (IC50=＜1nM) and ex19del/T790M), and can suppress activity of single gain-of-function mutant EGFR (including L858R and ex19del) as well. Mutated EGFR-IN-2 shows anti-tumor antivity .
Icenticaftor (QBW251) is an orally active CFTR channel potentiator, with EC50s of 79 nM and 497 nM for F508del and G551D CFTR, respectively. Icenticaftor can be used for chronic obstructive pulmonary disease (COPD) and cystic fibrosis research .
EGFR-IN-82 (Cmpound 8a) is a potent and orally active EGFR inhibitor with IC50 values of 0.09 and 0.06 nM for EGFR L858R/T790M/C797S and EGFR Del19/T790M/C797S, respectively. EGFR-IN-82 has no significant effect on EGFR WT. EGFR-IN-82 has anti-proliferative activity and inhibits tumor formation in nude mice. EGFR-IN-82 can be used in non-small cell lung cancer research .
Bamocaftor potassium is a cystic fibrosis transmembrane conductance regulator (CFTR) corrector designed to restore F508del-CFTR protein function. Bamocaftor potassium can be used combine with Tezacaftor (HY-15448) and Ivacaftor (HY-13017) in cystic fibrosis research .
PROTAC EGFR degrader 6, a PROTAC EGFR degrader, potently degrades EGFR Del19 in HCC827 cells with the DC50 of 45.2 nM. PROTAC EGFR degrader 6 significantly induces the apoptosis of HCC827 cells and arrest the cells in G1 phase .
HJM-561 is a selective and effective orally active EGFRPROTAC degrader. HJM-561 is able to overcome the triple EGFR mutations that are resistant to Osimertinib (HY-15772). HJM-561 exhibits potent degradation of EGFR Del19/T790M/C797S (DC50: 9.2 nM) and L858R/T790M/C797S (DC50: 5.8 nM), and has anti-tumor activity (pink: EGFR ligand (HY-12857); blue: CRBN ligand (HY-A0003); black: linker) .
PROTAC EGFR degrader 5 (Compound 10), a PROTAC EGFR degrader, potently degrades EGFR Del19 in HCC827 cells with the DC50 of 34.8 nM. PROTAC EGFR degrader 5 significantly induces the apoptosis of HCC827 cells and arrest the cells in G1 phase .
Bamocaftor (VX-659) is a cystic fibrosis transmembrane conductance regulator (CFTR) corrector designed to restore F508del-CFTR protein function. Bamocaftor can be used combine with Tezacaftor (HY-15448) and Ivacaftor (HY-13017) in cystic fibrosis research .
Ivacaftor-d18 is the deuterium labeled Ivacaftor . Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively .
EGFR-IN-23 is a potent EGFR TKI (tyrosine kinase inhibitor) with an IC50 of 8.05 nM for BaF3/EGFR-DEL19/T790M/C797S cell (WO2021244502A1, compound 8) .
Ivacaftor (Standard) is the analytical standard of Ivacaftor. This product is intended for research and analytical applications. Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively.
CFTR corrector 15 (Compound 4172) is a corrector for cystic fibrosis transmembrane conductance regulator (CFTR), that repairs the F508del-CFTR folding defect when used with VX-809 (HY-13262). CFTR corrector 15 can be used in research of cystic fibrosis disease .
BI-4732 a potent inhibitor EGFR-activating (E19del and L858R) and T790M mutations, with high blood-brian barrier penetration, targeting a broad range of EGFR mutations, including C797S. BI-4732 has anti-tumor activity .
EGFR-IN-158 (compound 12e) is an orally active EGFR inhibitor with an IC50 of 0.22 nM for EGFR(Del19/T790M). EGFR-IN-158 inhibits phosphorylation and downstream signaling by binding to EGFR, thereby inhibiting the proliferation of tumor cell lines and promoting apoptosis .
Gefitinib-based PROTAC 3, conjugating an EGFR binding element to a von Hippel-Lindau ligand via a linker, induces EGFR degradation with DC50s of 11.7 nM and 22.3 nM in HCC827(exon 19 del) and H3255 (L858R mutantion) cells, respectively .
EGFR-IN-97 (compound 6q) is a EGFR inhibitor. EGFR-IN-97 shows inhibitory activity against Ba/F3-EGFR L858R/T790M/C797S and Ba/F3-EGFR Del19/T790M/C797S cells, with IC50 values of 0.42 μM and 0.41 μM, respectively. EGFR-IN-97 can promote apoptosis of NCI-H1975-EGFR L858R/T790M/C797S cells at the concentration of 0.8 μM .
Ivacaftor- 13C6 (VX-770- 13C6) is 13C labeled Ivacaftor. Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively.
Ivacaftor-d4 (VX-770-d4) is the deuterium labeled-Ivacaftor (HY-13017). Ivacaftor is a potent and orally active CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively .
RNF5 agonist 1 (analog-1), a structural analog of RNF5 inhibitor inh-02 (HY-123967), is a potent RNF5 agonist. RNF5 agonist 1 increases the ubiquitylation status of ATG4B in F508del-CFTR-expressing CFBE41o- cells .
DA-0157 is the orally active inhibitor for EGFR and ALK that overcomes drug-resistant mutations of EGFR C797S and ALK in NSCLC) cells. DA-0157 inhibits the proliferation of Ba/F3-EGFR Del19/T790M/C797S (IC50 = 6.9 nM), Ba/F3-EGFR WT (IC50 = 0.83 μM), Ba/F3-EML4-ALK-L1196M (IC50 = 5.5 nM), and Ba/F3-EML4-ALK (IC50 = 7.4 nM). DA-0157 inhibits CYP2D6 with IC50 of 5.26 μM. DA-0157 exhibits antitumor efficacy in mouse models .
HG-14-10-04 is a potent ALK and mutant EGFR inhibitor with IC50s of 20 nM, 15.6 nM, 22.6 nM and 124.5 nM for ALK, EGFR LR/TM, EGFR 19del/TM/CS and EGFR LR/TM/CS, respectively. HG-14-10-04 can be used to research anticancer .
Zorifertinib (AZD3759) hydrochloride is a potent, orally active, central nervous system-penetrant, EGFR inhibitor (IC50s: 0.3, 0.2, and 0.2 nM for EGFR wt, EGFR L858R, and EGFR exon 19Del, respectively). Zorifertinib hydrochloride induces cancer cell apoptosis. Zorifertinib hydrochloride has antitumor activity, and can be used for NSCLC, HCC etc. research .
LS-106 is an orally active and potent inhibitor against epidermal growth factor receptor (EGFR) . LS-106 exhibits antitumor activities both in vitro and in vivo. LS-106 inhibits the kinase activities of EGFR19del/T790M/C797S and EGFRL858R/T790M/C797S with IC50 values of 2.4 nmol/L and 3.1 nmol/L, respectively, which is more potent than Osimertinib (HY-15772). LS-106 induces Apoptosis, suppresses cell proliferation of tumor cells harboring EGFR 19del/T790M/C797S and leas to significant tumor regression in a C797S-mutant xenograft model .
Zorifertinib (AZD3759) is a potent, orally active, central nervous system-penetrant, EGFR inhibitor. At Km ATP concentrations, the IC50s are 0.3, 0.2, and 0.2 nM for EGFR wt, EGFR L858R, and EGFR exon 19Del, respectively. Zorifertinib induces cancer cell apoptosis. Zorifertinib has antitumor activity, and can be used for NSCLC, HCC etc. research .
EMI1 is an EGFR ex19del/T790M/C797S and EGFR L858R/T790M/C797S inhibitor. EMI1 can be used for the research of mutant EGFR-associated, drug-resistant non-small-cell lung cancer (NSCLC) .
EGFR-IN-154 (compound 4c) is an EGFR inhibitor with EC50 values of 0.16 μM, 21.73 μM and 41.56 μM against EGFR Del19, EGFR WT and EGFR L858R, respectively. EGFR-IN-154 shows anticancer activity on various cance cell lines. EGFR-IN-154 induces mitochondrial apoptosis, and decreases pERK1/2 and pAkt levels, but increases pJNK and pp38 levels .
EGFR-IN-91 (compound 9) is an orally available EGFR inhibitor with blood-brain barrier penetrability. EGFR-IN-91 inhibits EGFR L858R/C797S and EGFR exon 19del/C797S, inducing tumor regression in xenograft (PDX) mouse models. EGFR-IN-91 has the potential to inhibit localized and metastatic non-small cell lung cancer (NSCLC) driven by EGFR mutants .
PROTAC EGFR degrader 4 is a potent PROTAC targeting mutant EGFR.PROTAC EGFR degrader 4 induces EGFR del19 and EGFR L858R/T790M degradation with DC50s of 0.51 and 126 nM, respectively. PROTAC EGFR degrader 4 significantly inhibits growth of HCC827 and H1975 cell lines with IC50s of 0.83 and 203.1 nM, respectively. Induced EGFR degradation is related to autophagy .
PGD97 is a selective cyclic peptide inhibitor against CAL/CFTR interactions, with a KD value of 6 nM towards the CAL PDZ domain for its desulfide cyclized form. PGD97 (desulfide cyclized form) has selectivity ≥ 130-fold compared to NHERF1/2 PDZ domains. PGD97 is capable of stabilizing F508del-CFTR at the cell membrane and improving CFTR function required for proper fluid homeostasis in tne lung. PGD97 can be used for the research of cystic fibrosis .
PRMT5-MTA-IN-1 (Compound A9a) is an inhibitor for protein arginine methyltransferase PRMT5-MTA. PRMT5-MTA-IN-1 inhibits the proliferation of colorectal cancer cell HCT116 wildtype and MTAP del mutant, with an IC50 of 16 nM and 2.47 μM. PRMT5-MTA-IN-1 exhibits good liver microsomal stability and film permeability. PRMT5-MTA-IN-1 exhibits good pharmacokinetic characteristics in CD-1 mice .
Almonertinib (HS-10296) mesylate is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib mesylate shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC50: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib mesylate is used for the research of the non-small cell lung cancer .
Almonertinib (HS-10296) is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC50: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib is used for the research of the non-small cell lung cancer .
Almonertinib (HS-10296) hydrochloride is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib hydrochloride shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC50: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib hydrochloride is used for the research of the non-small cell lung cancer .
EGFR-IN-69 (compound 17g) is a potent EGFR inhibitor, with IC50 values of 4.3, 6.6 and 25.6 nM against EGFR L858R/T790M/C797S, EGFR L858R/T790M, and EGFR 19del/T790M/C797S, respectively. EGFR-IN-69 can be used for non-small-cell-lung-cancer (NSCLC) research .
EGFR-IN-1671 is a selective EGFR inhibitor with an IC50 of 0.19 nM. EGFR-IN-167 exhibits good potency against various EGFR mutants (IC50 = 0.109 nM, 0.75 nM and <0.05 nM against EGFR (L858R), EGFR (C797S) and EGFR (del19), respectively). EGFR-IN-1671 covalently engages the catalytically conserved lysine of EGFR in live mammalian cells. EGFR-IN-1671 demonstrates excellent anti-proliferative activity by inhibiting EGFR autophosphorylation. EGFR-IN-1671 can be used for the study of non-small-cell lung carcinomas (NSCLC), glioblastoma and many solid tumors .
Almonertinib (Standard) is the analytical standard of Almonertinib. This product is intended for research and analytical applications. Almonertinib (HS-10296) is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC50: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib is used for the research of the non-small cell lung cancer .
EGFR-IN-117 (Compound 8h) exhibits inhibitory activity against EGFR mutation, targets the tumor environment, and induces apoptosis of cancer cells. EGFR-IN-117 inhibits proliferations of H1975, PC-9, and EGFR mutant cells BaF3-EGFR L858R/T790M/C797S and BaF3– C797S/Del19/T790M, with IC50 of 13 nM, 19 nM, 1.2 nM and 1.3 nM, respectively. EGFR-IN-117 exhibits antitumor efficacy in mouse models .
PRMT5-MTA-IN-3-d3 (compound P22) is the deuterium labeled PRMT5-MTA-IN-3 (HY-172733). PRMT5-MTA-IN-3-d3 is an orally active PRMT5-MTA inhibitor. PRMT5-MTA-IN-3-d3 has antiproliferative effects on HTC116-MTAP del and wild type colorectal cancer HCT-116 cell lines, with IC50 values of 6 nM and 961 nM, respectively. PRMT5-MTA-IN-3-d3 has anticancer effects, especially for MTAP-deficient tumors, such as non-small cell lung cancer (NSCLC), pancreatic cancer .
PGD97 is a selective cyclic peptide inhibitor against CAL/CFTR interactions, with a KD value of 6 nM towards the CAL PDZ domain for its desulfide cyclized form. PGD97 (desulfide cyclized form) has selectivity ≥ 130-fold compared to NHERF1/2 PDZ domains. PGD97 is capable of stabilizing F508del-CFTR at the cell membrane and improving CFTR function required for proper fluid homeostasis in tne lung. PGD97 can be used for the research of cystic fibrosis .
Ivacaftor-d9 is a potent CFTR modulator and exhibits an EC50 value of 255 nM for CFTR potentiation in G551D/F508del HBE Cells. Ivacaftor-D9 acts as an orally active and improved deuterated Ivacaftor analog for cystic fibrosis research .
Tezacaftor-d4 (VX-661-d4) is the deuterium-labeled Tezacaftor (HY-15448), a F508del CFTR corrector. Tezacaftor helps CFTR protein reach the cell surface .
Ivacaftor-d4 (VX-770-d4) is the deuterium labeled-Ivacaftor (HY-13017). Ivacaftor is a potent and orally active CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively .
Ivacaftor-d9 is a potent CFTR modulator and exhibits an EC50 value of 255 nM for CFTR potentiation in G551D/F508del HBE Cells. Ivacaftor-D9 acts as an orally active and improved deuterated Ivacaftor analog for cystic fibrosis research .
Tezacaftor-d6 (VX-661-d6) is deuterium labeled Tezacaftor. Tezacaftor (VX-661) is a F508del CFTR corrector. It helps CFTR protein reach the cell surface. However, Ivacaftor (VX-770, HY-13017), a CFTR potentiator, helps to prolong the opening time of cell surface CFTR protein channels. Tezacaftor combining with Ivacaftor, shows potent efficacy against cystic fibrosis and diseases with homozygous for the CFTR Phe508del mutation. Moreover, Elexacaftor (VX-445, HY-111772) is also a CFTR corrector. Elexacaftor-Tezacaftor-Ivacaftor aims at with cystic fibrosis (CF) with at least one Phe508del mutation, often avoids the indication for lung transplantation .
Ivacaftor-d18 is the deuterium labeled Ivacaftor . Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively .
Ivacaftor- 13C6 (VX-770- 13C6) is 13C labeled Ivacaftor. Ivacaftor (VX-770) is a potent and orally bioavailable CFTR potentiator, targeting G551D-CFTR and F508del-CFTR with EC50s of 100 nM and 25 nM, respectively.
PRMT5-MTA-IN-3-d3 (compound P22) is the deuterium labeled PRMT5-MTA-IN-3 (HY-172733). PRMT5-MTA-IN-3-d3 is an orally active PRMT5-MTA inhibitor. PRMT5-MTA-IN-3-d3 has antiproliferative effects on HTC116-MTAP del and wild type colorectal cancer HCT-116 cell lines, with IC50 values of 6 nM and 961 nM, respectively. PRMT5-MTA-IN-3-d3 has anticancer effects, especially for MTAP-deficient tumors, such as non-small cell lung cancer (NSCLC), pancreatic cancer .
MEF2C Antibody (YA4192) is a mouse-derived and non-conjugated IgG1 antibody, targeting to MEF2C. It can be applicated for WB, IHC-P, FC, ELISA assays, in the background of human, mouse, rat, rabbit, monkey.
BMPR1A Antibody (YA3984) is a mouse-derived and non-conjugated IgG1 antibody, targeting to BMPR1A. It can be applicated for IHC-P, FC, ELISA assays, in the background of human.
FADK 1; FADK; FAK 1; FAK 1; FAK related non kinase polypeptide; FAK1; FAK1_HUMAN; Focal adhesion kinase 1; Focal adhesion kinase 1; Focal adhesion Kinase; Focal adhesion kinase isoform FAK Del33; Focal adhesion kinase related nonkinase; FRNK; p125FAK; pp125FAK; pp125FAK; PPP1R71; Protein phosphatase 1 regulatory subunit 71; Protein tyrosine kinase 2; Protein Tyrosine Kinase Cytoplasmic; Protein Tyrosine Kinase Cytoplasmic; Protein-tyrosine kinase 2; PTK 2; PTK 2; PTK2; PTK2 protein tyrosine kinase 2; PTK2 protein tyrosine kinase 2.
WB, ICC/IF
Human
FAK Antibody (YA5276) is a mouse-derived and non-conjugated monoclonal antibody, targeting to FAK. It can be applicated for WB, ICC/IF assays, in the background of human.
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