bleomycin

Bleomycin sulfate is a glycopeptide antibiotic with antitumor activity. It is commonly used as a DNA-damaging agent and DNA synthesis inhibitor. It functions by inducing DNA strand breaks without affecting RNA strands. Bleomycin sulfate is widely used in cancer research and for establishing pulmonary fibrosis animal models.

Bleomycin hydrochloride is a glycopeptide antibiotic and a DNA synthesis inhibitor. Bleomycin Sulfate can cause DNA strand breaks but not RNA strand breaks. Bleomycin Sulfate has anti-tumor activity.

Bleomycin Free Base is a complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.

Bleomycin B4 (Phleomycin F), an antibiotic with antitumor properties, is utilized in cancer research [1] [2] [3].

Demethyl bleomycin A2, a Bleomycin congener, exhibits DNA cleavage that is insensitive to the presence of 5-Methylcytidine [1].

Bleomycin A5 (Pingyangmycin), a glycopeptide antibiotic that is orally active, functions as an antineoplastic agent, an apoptosis inducer, and a bacterial metabolite [1] [2].

Bleomycin B2 (Phleomycin D2) is an anticancer agent that targets DNA. It induces DNA strand breaks, thereby inhibiting the growth and proliferation of cancer cells. Bleomycin B2 holds promise for cancer research.

Bleomycin A6 (also known as boanmycin) is utilized in trials for treating squamous cell lung cancer. Studies indicate that Bleomycin A6 not only exhibits antitumor effects but also modifies the tumor microenvironment, which may contribute to the recurrence and metastasis of lung cancer during prolonged treatment.

Bleomycin A2 is an antibiotic that promotes DNA degradation and is also an AspH (aspartate/asparagine-β-hydroxylase) inhibitor (IC50 = 1.47 μM), with anti-tumor activity.

Deglycobleomycin is an RNA cleaving agent that targets r(CUG) repeat sequences. By binding with small molecules that recognize r(CUG)exp, Deglycobleomycin can selectively cleave r(CUG)exp. Its efficiency in cleaving DNA is considerably lower than that of Bleomycin A5(Pingyangmycin), but it exhibits enhanced selectivity for r(CUG)exp. Deglycobleomycin is useful for research on diseases associated with r(CUG) repeat expansions, such as myotonic dystrophy type 1, and the development of drugs aimed at precise targeting and cleavage of pathogenic RNA.

N1-Acetylspermine trihydrochloride is a monoacetylated derivative of spermine which is an endogenous polyamine. N1-Acetylspermine trihydrochloride can be used in studies about the uptake of the anticancer polyamine analog bleomycin-A5 by the human carnitine transporter SLC22A16.

3-CPs (3-Carbethoxypsoralen) is a bleomycin-induced serotypic podoplanar polysaccharide in mouse lung fibrosis that belongs to the psoralen family and interferes with antibody-mediated bacterial killing.3-CPs delays bleomycin-induced lung fibrosis in mice and can be used in studies of airway inflammation and asthma.

CCG-257081 (MRTF/SRF-IN-1) is an inhibitor of cardiac myosin-related transcription factor and serum response factor (MRTF/SRF) that acts by inhibiting the Rho/MRTF/SRF pathway.CCG-257081 has shown efficacy in preventing bleomycin-induced fibrosis in several mouse models. CCG-257081 can be used in cancer prevention and fibrosis research.

Aucuparin (2,6-dimethoxy-4-phenylphenol) is a plant antibiotic with anti-inflammatory activity. Aucuparin inhibited pulmonary fibrosis in mouse models induced by bleomycin (BLM). ABTS and FRAP showed clear scavenging activity. Aucuparin inhibited superoxide production of human neutrophils induced by fmlp, and its IC50 was 17.0μM.

Kasugamycin hydrochloride (Kasumin) is an aminoglycoside antibiotic that was originally isolated in 1965, from Streptomyces kasugaensis, a Streptomyces strain found near the Kasuga shrine in Nara, Japan. Kasugamycin hydrochloride was discovered by Hamao Umezawa, who also discovered kanamycin and bleomycin, as a drug which could prevent growth of a fungus causing rice blast disease.

CLT-28643 is a potent and specific α5β1-Integrin inhibitor that prevents fibrosis in glaucoma filtration surgery (GFS), inhibits tumor growth and angiogenesis, suppresses fibrosis and inflammation in a bleomycin-induced lung fibrosis model, and improves insulin sensitivity and cardiac function in H9C2 cells from obese mice.

Neotuberostemonine (NTS) is one of the main antitussive alkaloids in the root of Stemona tuberosa Lour, it has a significant protective effect on bleomycin (BLM)-induced pulmonary fibrosis through suppressing the recruitment and M2 polarization of macroph

TP-DEA2, a prodrug of triptolide, effectively inhibits bleomycin-induced pulmonary fibrosis and inflammatory responses. It significantly reduces the production of α-SMA.

JNK-1-IN-4 (Compound E1) is an inhibitor of JNK, targeting JNK-1, JNK-2, and JNK-3 with IC50 values of 2.7, 19.0, and 9.0 nM, respectively. This compound inhibits the phosphorylation of c-Jun and reduces the expression of TGF-β1-induced EMT markers (such as fibronectin and α-SMA). JNK-1-IN-4 exhibits favorable pharmacokinetic properties with a bioavailability of 69%. Additionally, it demonstrates antifibrotic effects in a Bleomycin-induced mouse model of idiopathic pulmonary fibrosis.

MORF-627 is an orally active selective inhibitor of integrin αvβ6 (integrinαvβ6), with an IC50 of 9.2 nM as measured in a human serum ligand binding assay. It effectively inhibits αvβ6-mediated activation of TGF-β1 with an IC50 of 2.63 nM and suppresses SMAD2/3 phosphorylation, showing an IC50 of 8.3 nM. Additionally, MORF-627 ameliorates bleomycin-induced pulmonary fibrosis in mice.

PDE1-IN-8 (Compound 3f) acts as an inhibitor of PDE1, with an IC50 of 11 nM. It hinders cAMP and cGMP signaling pathways, impeding the differentiation and proliferation of cells into myofibroblasts, and demonstrates antifibrotic effects in the Bleomycin-induced rat model of pulmonary fibrosis.

TRPV1-IN-3 (compound 14) is a TRPV1 inhibitor utilized in idiopathic pulmonary fibrosis research. It demonstrates antifibrotic activity in vitro (IC50 = 0.51 μM) by inhibiting the TGF-β/Smads and MAPK pathways, thereby affecting the expression of fibrosis markers collagen I and α-SMA. In vivo, TRPV1-IN-3 significantly reduces collagen deposition in lung tissue, improves alveolar structure, and increases survival rates in mice with Bleomycin-induced pulmonary fibrosis.

FGFRs-IN-1 (Compound A16) is an orally active inhibitor targeting FGFR1/2/3/4, with IC50 values of 2.3, 7, 11, and 163 nM respectively. It also inhibits VEGFR1/2/3, Abl, and Flt3, with IC50 values of 61, 176, 112, 26, and 353 nM. The compound shows weak inhibition of CYP enzymes. FGFRs-IN-1 reduces the expression of α-SMA and collagen I, and it inhibits epithelial-mesenchymal transition (EMT) in A549 cells stimulated by TGF-β1. Additionally, FGFRs-IN-1 demonstrates anti-inflammatory activity in mouse models of lung fibrosis induced by Bleomycin and liver fibrosis induced by CCl4.

ATX inhibitor 25 (Compound 29) is an orally active Autotaxin inhibitor with an IC50 of 1.08 nM. It exhibits excellent in vitro metabolic stability, with a half-life (t1/2) of over 170 minutes. In a bleomycin-induced pulmonary fibrosis mouse model, ATX inhibitor 25 (administered orally) shows antifibrotic effects.