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Galicaftor (ABBV-2222; GLPG-2222) is a potent and orally active cysticfibrosis transmembrane conductance regulator (CFTR) corrector. Galicaftor can be used for cysticfibrosis research .
(R)-Olacaftor ((R)-VX-440) is a Cysticfibrosis transmembrane conductance regulator (CFTR) modulator. (R)-Olacaftor has good potential for the study of cysticfibrosis (CF) .
CFTR corrector 9 (compound 42) is a cysticfibrosis transmembrane conductance regulator (CFTR) modulator. CFTR corrector 9 can be used for researching cysticfibrosis (CF) and other CFTR associated disorders .
Posenacaftor (PTI-801) sodium is a cysticfibrosis transmembrane regulator (CFTR) protein modulator that corrects the folding and trafficking of CFTR protein. Posenacaftor sodium is used for the research of cysticfibrosis (CF) .
CFTR corrector 4 (Compound 13), an active (R,R)-form enantiomer, is a highly potent and orally active cysticfibrosis transmembrane conductance regulator (CFTR) corrector. CFTR corrector 4 can increase CFTR levels at the cell surface and have the potential for treatment of cysticfibrosis .
CFTR corrector 16 (Compound 39) is a corrector for cysticfibrosis transmembrane conductance regulator (CFTR), that can be used in research of cysticfibrosis disease .
GLPG-3221 is a potent, orally active corrector of CFTR (cysticfibrosis transmembrane conductance regulator), with an EC50 of 105 nM. GLPG-3221 can be uesd for the treatment of cysticfibrosis .
CFTR corrector 15 (Compound 4172) is a corrector for cysticfibrosis 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 cysticfibrosis disease .
Riselcaftor (Example 33) is a CFTR modulator, with an EC50 of 20.1 nM in human bronchial epithelial cells. Riselcaftor can be used for research of cysticfibrosis .
Posenacaftor (PTI-801) is a cysticfibrosis transmembrane regulator (CFTR) protein modulator that corrects the folding and trafficking of CFTR protein. Posenacaftor is used for the research of cysticfibrosis (CF) .
Corr4A is a chemical corrector, which can be used for cysticfibrosis. Corr4A interacts directly with the cysticfibrosis transmembrane conductance regulator (CFTR) or affects indirectly its folding process. Corr4A increases the expression of CFTR ΔF508 on the cell surface, thereby improving its transport to the plasma membrane and increasing the stability of the rescued mutant protein .
Elexacaftor (VX-445, Compound 1) is a modulator of cysticfibrosis transmembrane conductance regulator (CFTR). Elexacaftor (VX-445, Compound 1) facilitates the processing and trafficking of CFTR to increase the amount of CFTR at the cell surface .
(R)-Posenacaftor (R)-PTI-801) sodium is the R enantiomer of Posenacaftor. Posenacaftor is a cysticfibrosis transmembrane regulator (CFTR) protein modulator that corrects the folding and trafficking of?CFTR?protein. Posenacaftor is used for the research of cysticfibrosis (CF) .
CFTR corrector 14 (Compound SVQ26) is a class 3 corrector for cysticfibrosis transmembrane conductance regulator (CFTR), that promotes the CFTR activity (EC50 of 3.08 μM with presence of C1 class corrector VX-809). CFTR corrector 14 regulates the mutant-caused misfolding and impaired function of the CFTR protein. CFTR corrector 14 can be used in research about cysticfibrosis .
CFTR corrector 13 (SVQ18) is a cysticfibrosis transmembrane conductance regulator (CFTR) corrector (EC50=3.14 μM). CFTR corrector 13 enhances the function of CFTR channels, especially when used in combination with Lumacaftor (HY-13262), it can produce a dose-dependent increase in CFTR function. CFTR corrector 13 can be used in the study of cysticfibrosis (CF) and other CFTR-related diseases .
Bamocaftor potassium is a cysticfibrosis 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 cysticfibrosis research .
Bamocaftor (VX-659) is a cysticfibrosis 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 cysticfibrosis research .
CFTR corrector 6 is a potent potentiator of CysticFibrosis Transmembrane conductance Regulator (CFTR). CFTR corrector 6 has the potential for cysticfibrosis (CF) and other CFTR associated disorders research .
Vanzacaftor (VX-121) is an orally active noval corrector of Cysticfibrosis transmembrane conductance regulator (CFTR). Vanzacaftor improves processing and trafficking of CFTR protein as well as increases chloride transport in triple combined with Tezacaftor (HY-15448) and Deutivacaftor. Vanzacaftor-Tezacaftor-Deutivacaftor is safe and well tolerated, improving lung function, respiratory symptoms, and CFTR function with cysticfibrosis, which is promising for research in the field of cysticfibrosis diseases .
L-K6L9 shows antimicrobial and antibiofilm activities against P. aeruginosa from cysticfibrosis patients. L-K6L9 is stable and resistant to degradation by cysticfibrosis sputum proteases and will not induce bacterial resistance .
D-K6L9 shows antimicrobial and antibiofilm activities against P. aeruginosa from cysticfibrosis patients. D-K6L9 is stable and resistant to degradation by cysticfibrosis sputum proteases and will not induce bacterial resistance .
NJH-2-056 is a deubiquitinase-targeting chimera (DUBTAC) linking the OTUB1 recruiter EN523 to the CFTR chaperone lumacaftor. NJH-2-056 can be used for cysticfibrosis research .
Cavosonstat (N91115) is an orally active S-nitrosoglutathione reductase (GSNOR) inhibitor. Cavosonstat is a CFTR stabilizer, and can be used for cysticfibrosis 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 cysticfibrosis research[1].
Dornase alfa (rhDNase) is a recombinant human deoxyribonuclease I (rhDNase), an enzyme which selectively cleaves DNA. Dornase alfa hydrolyzes the DNA present in sputum/mucus and reduces viscosity in the lungs, promoting improved clearance of secretions. Dornase alfa plays an important role in cysticfibrosis .
Duramycin (Moli1901) is a lantibiotic derived from Streptomyces cinnamoneuma. Duramycin also is a antimicrobial peptide. Duramycin can be used for the research of cysticfibrosis (CF) .
L-NBDNJ, a glycomimetic, is an antivirulence agent. L-NBDNJ interferes with the expression of proteins regulating cytoskeleton assembly and organization of the host cell. L-NBDNJ has anti-inflammatory and anti-infective effects in models of cysticfibrosis (CF) lung disease infection .
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 cysticfibrosis research .
SRI-41315 induces a prolonged pause at stop codons and suppresses PTCs (premature termination codons) associated with cysticfibrosis in immortalized and primary human bronchial epithelial cells, restoring CFTR (cysticfibrosis transmembrane conductance regulator) expression and function. SRI-41315 suppresses PTCs by reducing the abundance of the termination factor eRF1. SRI-41315 also potentiates aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity .
Cofirasersen is designed to reduce the expression of ENaC in the lung. ENaC is a sodium transport channel and believed to be hyperactive in cysticfibrosis, which is caused by mutations in the cysticfibrosis transmembrane regulator gene.
Cofirasersen sodium is designed to reduce the expression of ENaC in the lung. ENaC is a sodium transport channel and believed to be hyperactive in cysticfibrosis, which is caused by mutations in the cysticfibrosis transmembrane regulator gene.
Aloisine A (RP107) is a a potent cyclin-dependent kinase (CDK) inhibitor with IC50s of 0.15 μM, 0.12 μM, 0.4 μM, 0.16 μM for CDK1/cyclin B, CDK2/cyclin A, CDK2/cyclin E, CDK5/p35, respectively. Aloisine A ininhibits GSK-3α (IC50=0.5 μM) and GSK-3β (IC50=1.5 μM). Aloisine A stimulates wild-type CFTR and mutated CFTR, with submicromolar affinity by a cAMP-independent mechanism. Aloisine A has the potential for CFTR-related diseases, including cysticfibrosis research .
Talniflumate (BA 7602-06) is the proagent of Niflumic acid (HY-B0493), exerting its activity in the body through conversion to niflumic acid by esterase . Talniflumate is an orally active Ca 2+-activated Cl - channel (CaCC) blocker. Talniflumate can be used as an analgesic and anti-inflammatory agent in cysticfibrosis mouse model of distal intestinal obstructive syndrome .
Glibenclamide (Glyburide) is an orally active ATP-sensitive K + channel (KATP) inhibitor and can be used for the research of diabetes and obesity . Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR) . Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability . Glibenclamide can induce autophagy .
(R)-MDL-101146 is an orally active, competitive and reversible inhibitor against human neutrophil elastase (HNE) with a Ki value of 25 nM. (R)-MDL-101146 inhibits HNE-induced hemorrhage in hamsters. (R)-MDL-101146 is promising for research of emphysema, rheumatoid arthritis, chronic bronchitis, cysticfibrosis, adult respiratory distress syndrome and glomerulonephritis .
(S)-MDL-101146 is an orally active, competitive and reversible inhibitor against human neutrophil elastase (HNE) with a Ki value of 25 nM. (S)-MDL-101146 inhibits HNE-induced hemorrhage in hamsters. (S)-MDL-101146 is promising for research of emphysema, rheumatoid arthritis, chronic bronchitis, cysticfibrosis, adult respiratory distress syndrome and glomerulonephritis .
Glibenclamide (Standard) is the analytical standard of Glibenclamide. This product is intended for research and analytical applications. Glibenclamide (Glyburide) is an orally active ATP-sensitive K + channel (KATP) inhibitor and can be used for the research of diabetes and obesity . Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR) . Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability . Glibenclamide can induce autophagy .
KM11060 is a corrector of the F508 deletion (F508del)-cysticfibrosis transmembrane conductance regulator (CFTR) trafficking defect. KM11060 can be used for the research of F508del-CFTR processing defect and development of cysticfibrosis research .
I1421 is an activator of the cysticfibrosis transmembrane conductance regulator (CFTR) with an EC50 of 64 nM for WT CFTR currents. I1421 also allosterically activates multiple mutants causing cysticfibrosis (CF) with good in vivo potency, with an oral bioavailability of 60% in mice corresponding to a half-life of 75 min. I1421 synergizes with Elexacaftor (HY-111772) to enhance CFTR currents .
Phenamil methanesulfonate, an analog of Amiloride (HY-B0285), is a more potent and less reversible epithelial sodium channel (ENaC) blocker with an IC50 of 400 nM . Phenamil methanesulfonate is also a competive inhibitor of TRPP3 and inhibits TRPP3-mediated Ca 2+ transport with an IC50 of 140 nM in a Ca 2+ uptake assay . Phenamil methanesulfonate is an intriguing small molecule to promote bone repair by strongly activating BMP signaling pathway . Phenamil methanesulfonate is used for the research of cysticfibrosis lung disease .
GLPG2451 is a cysticfibrosis transmembrane conductance regulator (CFTR) potentiator, which effectively potentiates low temperature rescued F508del CFTR with an EC50 of 11.1 nM .
(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 cysticfibrosis .
Lonodelestat (POL6014) is a potent, orally active and selective peptide inhibitor of human neutrophil elastase (hNE). Lonodelestat (POL6014) has the potential for the research of cysticfibrosis (CF) .
Lonodelestat TFA (POL6014 TFA) is a potent, orally active and selective peptide inhibitor of human neutrophil elastase (hNE). Lonodelestat TFA has the potential for the research of cysticfibrosis (CF) .
Exaluren (ELX-02) is an synthetic eukaryotic ribosome-selective glycoside that induces read through of nonsense mutations, resulting in normally localized full-length functional proteins. Exaluren is used for the research of cysticfibrosis caused by nonsense mutations .
LasR-IN-2 is a LasR inhibitor that forms H-bonding with TRY-56 residue. LasR-IN-2 can be used in the research of bacterial infection, neutropenia, severe burns and chronic lung disease in cysticfibrosis (CF) .
Auraptene is an orally active geranyloxycoumarin that can be isolated from plants in the Brassicaceae family, antibacterial, anti-pathogen, antioxidant, anti-tumor, and neuroprotective effects. Auraptene plays an important role in the treatment of various chronic diseases such as hypertension and cysticfibrosis[1][2].
(R)-Elexacaftor is an enantiomer of Elexacaftor (HY-111772). (R)-Elexacaftor is the Compound 37 from patent WO2018107100A1. (R)-Elexacaftor is a modulator of cysticfibrosis transmembrane conductance regulator (CFTR), the EC50 for CFTR dF508 is 0.29 uM .
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 cysticfibrosis 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 cysticfibrosis (CF) with at least one Phe508del mutation, often avoids the indication for lung transplantation .
GSK199 analog hydrochloride belongs to a class of compounds that inhibit PAD4 (guanidinoarginine deiminase 4). GSK199 analog hydrochloride has potential uses in diseases including rheumatoid arthritis, vasculitis, systemic lupus erythematosus, ulcerative colitis, cancer, cysticfibrosis, asthma, cutaneous lupus erythematosus, and psoriasis .
PAD-IN-2 is a potent pad4 inhibitor (IC50: <1 μM). PAD-IN-2 can be used in the research of auto-immune diseases and cancers, such as rheumatoid arthritis, vasculitis, systemic lupus erythematosis, cutaneous lupus erythematosis, ulcerative colitis, cysticfibrosis, asthma, multiple sclerosis and psoriasis .
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 cysticfibrosis research .
VRT-532 (CFpot-532) is a potent is a potent CFTR modulator. VRT-532 enhances channel activity in G551D-CFTR and intrinsic ATPase activity of G551D-CFTR. VRT-532 has the potential for the research of cysticfibrosis .
Auraptene (Standard) is the analytical standard of Auraptene. This product is intended for research and analytical applications. Auraptene is an orally active geranyloxycoumarin that can be isolated from plants in the Brassicaceae family, antibacterial, anti-pathogen, antioxidant, anti-tumor, and neuroprotective effects. Auraptene plays an important role in the treatment of various chronic diseases such as hypertension and cysticfibrosis .
VRT-325 is a novel small molecule discovered by screening a compound library designed to address the genetic defect in cysticfibrosis (CF) caused by the ΔF508 mutation in CFTR. VRT-325 belongs to a class of compounds that promote ΔF508-CFTR efflux from the endoplasmic reticulum and restores chloride transport levels in epithelial cells of CF-derived bronchi .
PC190723 (Compound 2) is an inhibitor of the bacterial cell division protein FtsZ with an IC50 of 55 ng/ml. FtsZ-IN-3 exhibits anti-staphylococcal activity with MIC values of 1 µg/ml for MSSA and MRSA .
Glyburide-d11 is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
Glyburide-d3 is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cysticfibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle .
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 cysticfibrosis research .
GSK-2793660 (free base) is an oral, irreversible inhibitor of Cathepsin C (CTSC). GSK-2793660 (free base) can be used for the research of bronchiectasis .
1-Thioglycerol, commonly used as a reducing agent in various biochemical and biophysical applications, especially in protein chemistry and molecular biology, it can protect proteins from oxidation and denaturation, and can reduce disulfide bonds to thiols base, which can then be modified or analyzed. In addition, 1-Thioglycerol has been investigated for potential medical applications, including as an inhibitor of cysticfibrosis, which may help improve the function of lung cells, and has also been studied for Used in the preparation of metal nanoparticles and as a stabilizer for certain pharmaceutical preparations.
PAT1inh-A0030 is a selective PAT1 (SLC26A6) inhibitor (IC50= 1.0 μM). PAT1inh-A0030 inhibits fluid absorption in the ileum of wild-type and cysticfibrosis (CF) mice (CftrdelF508/delF508) in a closed-loop model of intestinal fluid absorption. PAT1inh-A0030 can be used in the study of intestinal diseases related to CF .
2'-Aminoacetophenone (Standard) is the analytical standard of 2'-Aminoacetophenone. This product is intended for research and analytical applications. 2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cysticfibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle .
PG01 is a potent CFTR Cl - channel potentiator. PG01 can correct gating defects of CFTR mutants, is effective on b>E193K, G970R and G551D (CFTR mutants) with Kd values of 0.22 μM, 0.45 μM and 1.94 μM, respectively. PG01 is also effective on ΔF508 (Ka of 0.3 μM). PG01 increases ΔF508-CFTR Cl - current after adding Forskolin .
Ganglioside GM2 asialo (asialo-GM2) is a glycosphingolipid containing three monosaccharide residues and one fatty acid of variable chain length, but lacks the sialic acid residue present on ganglioside M2. Asialo-GM2 is found at low or undetectable levels in normal human brains, but it accumulates in the brains of patients with Tay-Sachs disease and Sandhoff disease, which are expressed as lysosomal β- A neurodegenerative disorder characterized by hexosaminidase A and B deficiency. It also binds to various bacteria, including Pseudomonas isolated from cysticfibrosis patients. The Asialo-GM2 mixture contains ganglioside GM2 asialo molecular species with fatty acyl chains of variable length.
Mab-SaS-IN-1 (compoud 1H) is Mab-SaS inhibitor with the IC50 of 2 μM. Mab-SaS-IN-1 can be used for study of antibiosis by blocking iron uptake and metabolism .
IA-Alkyne (Iodoacetamide-alkyne; N-Hex-5-ynyl-2-iodo-acetamide) is a TRP channel (TRPC) agonist and has the potential for the study of respiratory infection . IA-Alkyne can be used to develop an isotopically tagged probe for quantitative cysteine-reactivity profiling . IA-Alkyne is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Ibuprofen (Standard) is the analytical standard of Ibuprofen. This product is intended for research and analytical applications. Ibuprofen ((±)-Ibuprofen) is a potent, orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen ((±)-Ibuprofen) can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
Ibuprofen- 13C6 ((±)-Ibuprofen- 13C6) is a 13C labeled Ibuprofen (HY-78131). Ibuprofen ((±)-Ibuprofen) is a potent, orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen ((±)-Ibuprofen) can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
Ibuprofen ((±)-Ibuprofen) is a potent, orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen ((±)-Ibuprofen) can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
Ibuprofen ((±)-Ibuprofen) sodium is an orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen sodium inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen sodium is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen sodium can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
Ibuprofen ((±)-Ibuprofen) L-lysine is a potent orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen L-lysine inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen L-lysine is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen L-lysine can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
1-Thioglycerol, commonly used as a reducing agent in various biochemical and biophysical applications, especially in protein chemistry and molecular biology, it can protect proteins from oxidation and denaturation, and can reduce disulfide bonds to thiols base, which can then be modified or analyzed. In addition, 1-Thioglycerol has been investigated for potential medical applications, including as an inhibitor of cysticfibrosis, which may help improve the function of lung cells, and has also been studied for Used in the preparation of metal nanoparticles and as a stabilizer for certain pharmaceutical preparations.
Ganglioside GM2 asialo (asialo-GM2) is a glycosphingolipid containing three monosaccharide residues and one fatty acid of variable chain length, but lacks the sialic acid residue present on ganglioside M2. Asialo-GM2 is found at low or undetectable levels in normal human brains, but it accumulates in the brains of patients with Tay-Sachs disease and Sandhoff disease, which are expressed as lysosomal β- A neurodegenerative disorder characterized by hexosaminidase A and B deficiency. It also binds to various bacteria, including Pseudomonas isolated from cysticfibrosis patients. The Asialo-GM2 mixture contains ganglioside GM2 asialo molecular species with fatty acyl chains of variable length.
Lonodelestat (POL6014) is a potent, orally active and selective peptide inhibitor of human neutrophil elastase (hNE). Lonodelestat (POL6014) has the potential for the research of cysticfibrosis (CF) .
Lonodelestat TFA (POL6014 TFA) is a potent, orally active and selective peptide inhibitor of human neutrophil elastase (hNE). Lonodelestat TFA has the potential for the research of cysticfibrosis (CF) .
L-K6L9 shows antimicrobial and antibiofilm activities against P. aeruginosa from cysticfibrosis patients. L-K6L9 is stable and resistant to degradation by cysticfibrosis sputum proteases and will not induce bacterial resistance .
D-K6L9 shows antimicrobial and antibiofilm activities against P. aeruginosa from cysticfibrosis patients. D-K6L9 is stable and resistant to degradation by cysticfibrosis sputum proteases and will not induce bacterial resistance .
C5aR1 antagonist peptide is a biological active peptide. (This linear peptide is derived from the C-terminus of the chemokine, complement fragment 5 anaphylatoxin (C5a). This peptide functions to inhibit C5a binding and function at human and rat C5a receptors. C5a is crucial to triggering cellular immune responses and its overexpression is involved in arthritis, Alzheimer’s disease, cysticfibrosis, systemic lupus erythematosus, and other immunoinflammatory diseases.)
Duramycin (Moli1901) is a lantibiotic derived from Streptomyces cinnamoneuma. Duramycin also is a antimicrobial peptide. Duramycin can be used for the research of cysticfibrosis (CF) .
Auraptene is an orally active geranyloxycoumarin that can be isolated from plants in the Brassicaceae family, antibacterial, anti-pathogen, antioxidant, anti-tumor, and neuroprotective effects. Auraptene plays an important role in the treatment of various chronic diseases such as hypertension and cysticfibrosis[1][2].
2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cysticfibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle .
Auraptene (Standard) is the analytical standard of Auraptene. This product is intended for research and analytical applications. Auraptene is an orally active geranyloxycoumarin that can be isolated from plants in the Brassicaceae family, antibacterial, anti-pathogen, antioxidant, anti-tumor, and neuroprotective effects. Auraptene plays an important role in the treatment of various chronic diseases such as hypertension and cysticfibrosis .
2'-Aminoacetophenone (Standard) is the analytical standard of 2'-Aminoacetophenone. This product is intended for research and analytical applications. 2'-Aminoacetophenone is an orally active inducer of apoptosis and respiratory biomarker. 2'-Aminoacetophenone can be used to detect Pseudomonas aeruginosa infections in the lungs of cysticfibrosis patients. 2'-Aminoacetophenone can inhibit the protein levels of LC3BII and p62 in macrophages infected with pqsA or mvfR and regulate autophagy. 2'-Aminoacetophenone can disrupt mitochondrial function by inducing oxidative stress and apoptosis signaling, leading to dysfunction in mouse skeletal muscle .
S100A8 consists of calcium and zinc bound S100A8, which plays a critical regulatory role in inflammation and immune responses. As calprotectin, it contributes to leukocyte function, regulates the cytoskeleton, and activates intracellular NADPH oxidase. S100A8 Protein, Human (C-His) is the recombinant human-derived S100A8 protein, expressed by E. coli , with C-6*His labeled tag. The total length of S100A8 Protein, Human (C-His) is 93 a.a., with molecular weight of ~13.0 kDa.
S100A8 consists of calcium and zinc bound S100A8, which plays a critical regulatory role in inflammation and immune responses. As calprotectin, it contributes to leukocyte function, regulates the cytoskeleton, and activates intracellular NADPH oxidase. S100A8 Protein, Human (N-His) is the recombinant human-derived S100A8 protein, expressed by E. coli , with N-6*His labeled tag. The total length of S100A8 Protein, Human (N-His) is 93 a.a., with molecular weight of ~12-13 kDa.
S100A8 consists of calcium and zinc bound S100A8, which plays a critical regulatory role in inflammation and immune responses. As calprotectin, it contributes to leukocyte function, regulates the cytoskeleton, and activates intracellular NADPH oxidase. S100A8 Protein, Human (sf9, His) is the recombinant human-derived S100A8 protein, expressed by Sf9 insect cells , with C-His labeled tag. The total length of S100A8 Protein, Human (sf9, His) is 93 a.a., with molecular weight of ~14.6 kDa.
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 cysticfibrosis research[1].
Glyburide-d3 is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
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 cysticfibrosis research .
Glyburide-d11 is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cysticfibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
Ibuprofen- 13C6 ((±)-Ibuprofen- 13C6) is a 13C labeled Ibuprofen (HY-78131). Ibuprofen ((±)-Ibuprofen) is a potent, orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen ((±)-Ibuprofen) can be used in the research of pain, swelling, inflammation, infection, immunology, cancers .
IA-Alkyne (Iodoacetamide-alkyne; N-Hex-5-ynyl-2-iodo-acetamide) is a TRP channel (TRPC) agonist and has the potential for the study of respiratory infection . IA-Alkyne can be used to develop an isotopically tagged probe for quantitative cysteine-reactivity profiling . IA-Alkyne is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
Cofirasersen is designed to reduce the expression of ENaC in the lung. ENaC is a sodium transport channel and believed to be hyperactive in cysticfibrosis, which is caused by mutations in the cysticfibrosis transmembrane regulator gene.
Cofirasersen sodium is designed to reduce the expression of ENaC in the lung. ENaC is a sodium transport channel and believed to be hyperactive in cysticfibrosis, which is caused by mutations in the cysticfibrosis transmembrane regulator gene.
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