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Pirfenidone

Pirfenidone is a small molecule drug used to treat idiopathic pulmonary fibrosis (IPF), a progressive and fatal lung disease.
It works by reducing inflammation and slowing the progression of fibrosis in the lungs.
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Its AI-driven comparisons enhance reproducibility and accuracy, ensuring researchers find the most effective Pirfenidone products and procedures.
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Most cited protocols related to «Pirfenidone»

1
Guidelines for Interstitial Lung Diseases
Cited 84 times
Methods including conflict-of-interest management were established a priori and are described in the online supplement. The document can be conceptualized in two parts. Narrative portions (e.g., radiological criteria, histopathological criteria, physiological criteria, definitions) were created using consensus by discussion. Guideline portions address specific questions related to TBLC, genomic classifier testing, antacid medication, antireflux surgery for IPF, and pirfenidone and nintedanib for PPF. These sections are compliant with the Institute of Medicine standards for trustworthy guidelines (6 ) and yield recommendations that were informed by systematic reviews and were formulated and graded using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) approach (7 (link)) (Table 1).
Evidence-based recommendations were formulated by discussion followed by voting. Briefly, committee members were provided the following options: a strong recommendation for a course of action, a conditional recommendation for a course of action, a conditional recommendation against a course of action, a strong recommendation against a course of action, and abstention (Table 2). Abstention was appropriate whenever a committee member was unwilling to commit for or against the proposed course of action, such as when there was insufficient evidence, or the committee member had insufficient expertise or a self-realized bias. Three outcomes were possible:
Raghu G., Remy-Jardin M., Richeldi L., Thomson C.C., Inoue Y., Johkoh T., Kreuter M., Lynch D.A., Maher T.M., Martinez F.J., Molina-Molina M., Myers J.L., Nicholson A.G., Ryerson C.J., Strek M.E., Troy L.K., Wijsenbeek M., Mammen M.J., Hossain T., Bissell B.D., Herman D.D., Hon S.M., Kheir F., Khor Y.H., Macrea M., Antoniou K.M., Bouros D., Buendia-Roldan I., Caro F., Crestani B., Ho L., Morisset J., Olson A.L., Podolanczuk A., Poletti V., Selman M., Ewing T., Jones S., Knight S.L., Ghazipura M, & Wilson K.C. (2022). Idiopathic Pulmonary Fibrosis (an Update) and Progressive Pulmonary Fibrosis in Adults: An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline. American Journal of Respiratory and Critical Care Medicine, 205(9), e18-e47.
Publication 2022
Antacids Committee Members Dietary Supplements nintedanib Operative Surgical Procedures Pharmaceutical Preparations physiology pirfenidone X-Rays, Diagnostic
2
TPMS: Integrating Biological Networks
Cited 9 times
The TPMS technology employed has been previously described [12 (link)] and applied in different clinical areas with different objectives [8 (link), 9 (link), 13 (link)–18 (link)]. TPMS uses a human biological network that incorporates the available relationships (edges or links) between proteins (nodes) from a regularly updated in-house database drawn from public sources: KEGG [28 (link)], REACTOME [29 (link)], INTACT [30 (link)], BIOGRID [31 (link)], HPRD [32 (link)], and TRRUST [33 (link)].
Drug targets and indications were obtained from DrugBank [34 (link)]. The molecular description of the indications was obtained from a hand-curated collection of associations between biological processes and molecular effectors (defined as BED, Biological Effectors Database, from Anaxomics Biotech). The method uses an artificial neural network (ANN) to measure the potential relationship between the nodes of a network (i.e. proteins), grouped according to their association with a phenotype. The ANN algorithm provides a score (from 0 to 100%). Each score is associated with a probability (p-value) that the protein or group of proteins being evaluated, drug targets with molecular description of pathological processes, are functionally associated. Scores greater than 91% indicate a very strong relationship with a p-value below 0.01; scores between 76–91% have p-value between 0.01–0.05; scores between 40–76% have medium–strong relationship and p-value in the range 0.05–0.25; and a scores lower than 40% have p-values above 0.25.
Artigas L., Coma M., Matos-Filipe P., Aguirre-Plans J., Farrés J., Valls R., Fernandez-Fuentes N., de la Haba-Rodriguez J., Olvera A., Barbera J., Morales R., Oliva B, & Mas J.M. (2020). In-silico drug repurposing study predicts the combination of pirfenidone and melatonin as a promising candidate therapy to reduce SARS-CoV-2 infection progression and respiratory distress caused by cytokine storm. PLoS ONE, 15(10), e0240149.
Publication 2020
Biological Processes Biopharmaceuticals Drug Delivery Systems Homo sapiens Pathologic Processes Pharmaceutical Preparations Phenotype Proteins Synapsin I
3
Therapeutic Interventions for Bleomycin-Induced Lung Fibrosis
Cited 5 times
All animal models were performed twice and data was jointly analyzed.
All animals treated were included in the analysis. Interventions were not
blinded, but analysis of animal samples was. a)
Bleomycin-model:C57Bl/6, 9–12 weeks-old, female mice were
purchased (Taconic Biosciences, Hudson, NY). Knockout mice
(Dio2−/−),
Ppargc1a−/− and
Pink1−/− of C57/BL6 background
were obtained from Jackson Lab (Bar-Harbor, ME). As previously
published11 (link),53 (link) genetic deletion of either PINK1 or
PPARGC1A does not produce any endogenous lung phenotype and is not associated
with derangements of lung physiology.
Ppargc1a−/− and
Pink1−/− mice are not
embryonically lethal, they produce litters of appropriate Mendelian size, are
fertile and healthy and present with no gross morphology abnormalities. Mice
were anesthetized by placing them in a chamber having paper towels soaked with
40% isoflurane solution diluted with 1,2-propanediol. Mice were randomly
assigned to either intratracheal 1.5 U/kg of bleomycin (Hospira, IL) or
equivalent volume (50 μL) of 0.9% normal saline was administered
intratracheally as previously described54 (link),55 (link). To test
therapeutic efficacy of TH in bleomycin-induced established fibrosis we used
intraperitoneal T4 (T2376-Sigma Aldrich, 100μg/kg), or aerosolized T3
(T2877-Sigma Aldrich, 40 μg/kg). T4 was administered systemically at
days 10, 12, 14, 16 and mice were sacrificed on day 19, following
bleomycin-challenge. Aerosolized T3 was administered every other day at days
10–20 and mice were sacrificed on day 21. Dose regimens were based on
previously published protocols24 (link),56 (link). Equivalent
volumes of normal saline 0.9% were used as controls in all approaches.
For survival analysis we used a double dose of bleomycin (3.0 U/kg) and
administered aerosolized T3 (40 μg/kg) or normal saline 0.9% at
days at days 10–20 (established fibrosis) following challenge and
survival data was collected at day 21, respectively. Mice were randomly assigned
to receive either pirfenidone (100 mg/kg) or nintedanib (60 mg/kg) or vehicle
(0.9% saline) via oral gavage, as previously described57 , at days 10–20 (on a
daily basis) following bleomycin administration and mice were sacrificed at day
21. Aerosolized delivery of T3 was performed following a standardized protocol.
Briefly: T3 was diluted to a final concentration of 40 μg/kg in 6 ml of
PBS and suspension was aerosolized using a conventional aerosol nebulizer
(Omron) throughout a chamber that allowed simultaneous exposure of 8 mice for 30
minutes until mist stopped forming in the nebulizer chamber. b)
TGF-β1-induced lung fibrosis: Inducible lung targeted
TGF-β1-overexpressing triple transgenic mice
(CC10-rtTA-tTS-TGF-β1) generated as previously
described16 (link) were used.
Briefly: A triple transgenic system based on the tetracycline-controlled
transcriptional suppressor (tTS) and the reverse tetracycline transactivator
(rtTA) was constructed. In this system, the CC10 promoter constitutively drives
the expression of rtTA and tTS in a lung-specific fashion. In the absence of
dox, tTS binds to and actively suppresses the expression of the
tet-O–regulated TGF-β1 transgene. In the presence of dox, tTS is
released allowing the activating, dox binding rtTA to bind to the tet-O and
activate transgene expression. As expected induced TGF-β1– overexpression upon addition of doxycycline water on a daily basis
(days 0–20) caused airway and parenchymal fibrotic response as assessed
by increased lung collagen deposition indicated by hydroxyproline levels and
Masson Trichrome staining. Aerosolized T3 (40 μg/kg) or normal saline
0.9% was administered every other day on days 10–20 following
addition of doxycycline and mice where sacrificed on day 21. c) Sobiterome
therapeutic protocol: Sobiterome was provided by the laboratory of
Dr. Scanlan as previously described21 (link),58 (link). C57Bl/6,
9–12 weeks-old, female mice were randomly assigned to be challenged with
1.5 U/kg of bleomycin or equivalent volume of normal saline 0.9% at day
0. Mice were then randomly assigned to treatment with 5 mg/kg of sobiterome
diluted in 50 μL of normal saline 0.9% or vehicle (equivalent
volume of normal saline 0.9%) administered by oral gavage at days 10,
12, 14, 16 and 18 following bleomycin administration and mice were sacrificed on
day 21.
Yu G., Tzouvelekis A., Wang R., Herazo-Maya J.D., Ibarra G.H., Srivastava A., de Castro J.P., DeIuliis G., Ahangari F., Woolard T., Aurelien N., e Drigo R.A., Gan Y., Graham M., Liu X., Homer R.J., Scanlan T.S., Mannam P., Lee P.J., Herzog E.L., Bianco A.C, & Kaminski N. (2017). Thyroid hormone inhibits lung fibrosis in mice by improving epithelial mitochondrial function. Nature medicine, 24(1), 39-49.
Publication 2017
Animal Model Animals Animals, Transgenic Bleomycin Collagen Congenital Abnormality Doxycycline Females Fibrosis Gene Deletion Hydroxyproline Isoflurane Lung Mice, Knockout Mice, Laboratory Mice, Transgenic Nebulizers nintedanib Normal Saline Obstetric Delivery Phenotype pirfenidone PPARGC1A protein, human Propylene Glycol Pulmonary Fibrosis Tests, Pulmonary Function Tetracycline TGF-beta1 Trans-Activators Transgenes Treatment Protocols Tube Feeding
4
Murine and Human 3D Lung Tissue Culture
Cited 4 times
Human and murine 3D-LTCs and 4 mm-punches thereof were generated as previously described [25 (link), 28 (link)]. The amount of slices generated from one mouse lung varied between 18 and 25 slices, determining the amount of further downstream analysis. The 3D-LTCs were cultured in DMEM-F12 containing 0.1% FCS and 1% penicillin/streptomycin. 3D-LTCs obtained from mice subjected to PBS or Bleomycin were stimulated either with Nintedanib (0.1 μM, 1 μM, 10 μM) or Pirfenidone (100 μM, 500 μM, 2.5 mM) for 48 h.
Human 3D-LTCs were treated with a fibrosis cocktail (FC) consisting of TGF-β, Platelet-derived growth factor (PDGF)-AB, tumor necrosis factor (TNF)-α and Lysophosphatidic acid (LPA) [25 (link)]. Briefly, slices and 4-mm biopsy punches were treated with FC or control cocktail (CC) for 48 h followed by the co-treatment of Nintedanib (1 μM) or Pirfenidone (500 μM) with FC or CC for 72 h (Fig. 4a). Supernatants from punches were pooled for each condition and stored at − 80 °C for further analysis. A WST-1 assay was performed as previously described [25 (link)]. Punches were fixed with 4% paraformaldehyde (PFA) for 30 min and subsequently washed with 1 X DPBS. Slices were snap-frozen in liquid nitrogen and stored at − 80 °C.
Lehmann M., Buhl L., Alsafadi H.N., Klee S., Hermann S., Mutze K., Ota C., Lindner M., Behr J., Hilgendorff A., Wagner D.E, & Königshoff M. (2018). Differential effects of Nintedanib and Pirfenidone on lung alveolar epithelial cell function in ex vivo murine and human lung tissue cultures of pulmonary fibrosis. Respiratory Research, 19, 175.
Publication 2018
Biological Assay Biopsy Bleomycin Fibrosis Freezing Homo sapiens Lung lysophosphatidic acid Mus nintedanib Nitrogen paraform Penicillins pirfenidone platelet-derived growth factor AB Streptomycin TNF protein, human Transforming Growth Factor beta
5
Idiopathic Pulmonary Fibrosis Diagnosis and Prognosis
Cited 4 times
Patients were identified from review of the Bristol ILD Service multidisciplinary (MDT) team database and clinical records from September 1, 2007 to December 31, 2014. Inclusion criteria for this study were an MDT consensus diagnosis of IPF according to American Thoracic Society (ATS)/European Respiratory Society (ERS) criteria [1 (link)] made between these dates and ≥12 months of follow-up. Diagnoses made before publication of the 2011 criteria were reviewed at an MDT meeting for confirmation. Patients with a “working diagnosis” of IPF were diagnosed as such based on clinicoradiological parameters in the context of MDT discussion. Where a confident diagnosis could not be made, patients were referred for surgical lung biopsy following discussion of the risks and benefits of such an approach and considering the clinical condition of the patient, in accordance with national guidelines [18 ]. Ethical approval for this work was given by the East of England research ethics committee (reference 15/EE/0023).
Demographic data were collected in addition to all-cause mortality and use of pirfenidone. Computed tomography of the chest was classified as “definite” or “possible” UIP pattern. Where echocardiography was performed around the time of the first clinical assessment, incidence of pulmonary hypertension was noted. Initiation of long-term oxygen therapy (LTOT) was documented at the time of the first visit. This was initiated in accordance with national guidelines only for those patients with arterial oxygen tension of <7.3 kPa or <8 kPa in the presence of evidence of pulmonary hypertension [21 (link)]. Comorbidities, specifically those including past or current history of cancer or cardiac disease, were noted.
Pulmonary function and exercise testing were all performed in the same physiology department according to international criteria [22 (link), 23 (link)]. Results from all spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) and 6-min walk testing (6MWT) were collated over the follow-up period. Relative changes in FVC and DLCO were calculated, as suggested by Richeldiet al. [24 (link)]. Change in FVC and DLCO on follow-up were noted, in addition to subsequent trends in spirometry results. The minimal clinically important difference (MCID) for IPF of 5% was used [13 (link)]. Desaturation was defined as a fall in pulse oximetry on exertion of ≥4% to a level of <88%. Disease progression was defined as death, respiratory hospitalisation or a fall in FVC of >10%.
Sharp C., Adamali H.I, & Millar A.B. (2017). A comparison of published multidimensional indices to predict outcome in idiopathic pulmonary fibrosis. ERJ Open Research, 3(1), 00096-2016.
Publication 2017
Biopsy Chest Diagnosis Disease Progression Echocardiography Ethics Committees, Research Europeans Heart Diseases Lung Malignant Neoplasms Monoxide, Carbon Oximetry, Pulse Oxygen Patients physiology pirfenidone Pulmonary Hypertension Pulmonary Surgical Procedures Respiratory Rate Self Confidence Spirometry Therapies, Oxygen Inhalation Training Programs X-Ray Computed Tomography

Most recents protocols related to «Pirfenidone»

1
Antibacterial Activity of Resorcin[4]arene Cocrystals
Not available on PMC !

Example 6

3 mg/ml stock solutions of PFD, RsC1, RsC1-PFD (1:1 complex), RsC4, and RsC4-PFD (1:1 complex) were prepared in DMSO (bcoz host soluble in DMSO solution). From the stock, a working solution 4× (highest conc. for each compound in plate) was prepared in LB media. 50 uL of LB media was first added in each well (96 well plate). Then a 4× solution of the respective compound was added to the first row (A4-A12) except A1-A3 (Positive control/bacterial innoculum). Then, the 4× was serially diluted up to well G for all 3 compounds. (A-G). Then, a 50 uL aliquot of the 100-fold diluted bacterial inoculum was added in each test well. Individual test concentrations (in triplicate wells in a 96-well plate) for the given compounds were achieved by serial dilution by using LB medium. Total volume in each well is 100 uL. The final-test concentration range for the individual test compounds for C. acnes, S. aureus and P. aeruginosa are as follows: PFD, RsC1, RsC4, RsC1-PFD complex and RsC4-PFD complex (128-2 ug/mL). The results are shown in Table 6.

TABLE 6
Antibacterial activities of cocrystals and their individual components
TestMIC (μg/mL); GI (%)
compoundS. aureus (MU50)P. aeruginosa (BAMF)C. acnes
PFD128; 45128; 35128; 98
RsC1 16; 98 64; 47 64; 96
RsC1-PFD (1)  8; 99128; 43 16; 93
RsC4128; 52 64; 56128; 98
RsC4-PFD (2)128; 26128; 39128; 99
C. acnes: Cutibacterium acnes;
S. aureus: Staphylococcus aureus;
P. aeruginosa: Pseudomonas aeruginosa;
MIC: Minimum inhibitory concentration;
GI: Growth inhibition.
PFD: pirfenidone;
RsC1: C-methylresorcin[4]arene;
1:1 cocrystal of RsC1-PFD (1);
RsC4: C-butylresorcin[4]arene;
1:1 cocrystal of RsC4-PFD (2).

FIG. 1A shows a Job's plot constructed from the chemical shift change (Δδ) of the phenyl ring protons (#2) of PFD in 1H NMR spectra by varying the ratio between PFD and RsC4. FIG. 1B shows a Job's plot constructed from the chemical shift change (Δδ) of the aromatic protons (#C) of RsC4 in 1H NMR spectra by varying the ratio between PFD and RsC4.

Diffusion coefficient of PFD in equimolar mixture has changed drastically compared to PFD alone (above spectra, FIGS. 1A and 1B) which indicates the PFD bind to RsC4 in the mixture and diffuses at slower rate compared to PFD alone. The interaction between host and guest were loose/weak, therefore RsC4 and PFD peaks do not correspond to the same diffusion constant and have different position on the y axis. The diffusion coefficient of solvent ACN-d3 is 3.17×10-9. The broad, mobile OH proton at 7.7 ppm of host RsC4 has disappeared in the spectra. The y-axis is shown as log D.

FIG. 7 is a graph showing the antibacterial activity of PFD alone and RsC1-PFD complex against S. aureus. The percent on each bar indicates growth inhibition at a specific concentration (minimum inhibitory concentration). FIG. 8 is a graph showing the antibacterial activity of PFD alone and RsC1-PFD complex against P. aeruginosa. The percent on each bar indicates growth inhibition at a specific concentration (minimum inhibitory concentration). FIG. 9 is a Job's plot (NMR titration), Stoichiometry 1:1.

All documents cited are incorporated herein by reference; the citation of any document is not to be construed as an admission that it is prior art with respect to the present invention.

It is to be further understood that where descriptions of various embodiments use the term “comprising,” and/or “including” those skilled in the art would understand that in some specific instances, an embodiment can be alternatively described using language “consisting essentially of” or “consisting of.”

While particular embodiments of the present invention have been illustrated and described, it would be obvious to one skilled in the art that various other changes and modifications can be made without departing from the spirit and scope of the invention. It is therefore intended to cover in the appended claims all such changes and modifications that are within the scope of this invention.

US11858899B2. Complexation of pirfenidone with polyphenolic calixarene or resorcin[4]arenes (2024-01-02). University of Cincinnati [US]. Inventors: Harshita Kumari [US], Suchitra Panigrahi [US].
Patent 2024
2
Pirfenidone for Mild-Moderate IPF
Adult patients with a definite diagnosis of IPF and mild-to-moderate lung function
impairment who were naïve to pirfenidone or had been treated with pirfenidone less than 30
days prior to enrolment, were eligible for inclusion. Exclusion criteria were:
hypersensitivity against any ingredient of pirfenidone; concomitant use of fluvoxamine;
severe hepatic impairment or end-stage liver failure; severe renal impairment (creatinine
clearance <30 ml/min) or end-stage renal failure requiring dialysis, or enrolment in
interventional clinical trials. All patients were required to provide their written informed
consent prior to enrolment.
Schreiber J., Schütte W., Koerber W., Seese B., Koschel D., Neuland K, & Grohé C. (2024). Clinical course of mild-to-moderate idiopathic pulmonary fibrosis during therapy with pirfenidone: Results of the non-interventional study AERplus. Pneumologie (Stuttgart, Germany), 78(4), 236-243.
Publication 2024
3
Management of Immune Checkpoint Inhibitor-Related Pneumonia
All patients were diagnosed and treated according to the expert consensus on the diagnosis and treatment of immune checkpoint inhibitor-related pneumonia in lung cancer patients.
Symptomatic supportive treatment was provided for grade 1 ICIP with close follow-up evaluation. Intravenous administration of methylprednisolone (1–2 mg/kg/d) was administered first for grade 2 ICIP, followed by oral administration of methylprednisolone (1–2 mg/kg/d) after 48 to 72 hours. Steroid treatment was gradually tapered (10 mg/week) after the symptoms abated and imaging improved; the treatment course was > 6 weeks. Intravenous administration of methylprednisolone (2–4 mg/kg/d) was administered first for grade 3 and 4 ICIP, followed by oral administration of methylprednisolone (2–4 mg/kg/d) after 48 to 72 hours. Steroid treatment was gradually tapered (10 mg per week) after the symptoms abated and imaging improved; the treatment course was > 8 weeks. There were 30 cases in the glucocorticoid alone group and 15 cases in the glucocorticoid-pirfenidone group, in which pirfenidone (approval number: National Drug Approval H20133375; Beijing Kontine Pharmaceutical Co., Ltd., Beijing) was added to the steroid treatment. The treatment regimen consisted of pirfenidone (100 mg) administered thrice-daily for a duration of 7 days, followed by pirfenidone (200 mg) administered thrice-daily for 14 days. Maintenance pirfenidone therapy was then initiated at a dose of 300 mg administered thrice-daily.
Li Y., Huang H., Ye X., Zeng B., Huang F, & Chen L. (2024). A retrospective study of combination therapy with glucocorticoids and pirfenidone for PD-1 inhibitor-related immune pneumonitis. Medicine, 103(16), e37808.
Publication 2024
4
Pirfenidone and Metformin Attenuate Bleomycin-Induced Lung Fibrosis
Forty‐eight mice were randomly divided into six groups with eight mice in each group: the control group, BLM group, pirfenidone (PFD) group, metformin (MET) group, pirfenidone+MET group (PFD + MET), and NADPH oxidase 4 (NOX4) inhibitor diphenyleneiodonium chloride (DPI) group. Every group except the control group was given 1.5 U BLM (1.5 mg/kg; Nippon Kayaku Co., Tokyo, Japan) by endotracheal administration on Day 0. Beginning on Day 7, the PFD group was intragastrically administered pirfenidone (200 mg/kg body weight; Beijing Kangdini Pharmaceutical Co., Ltd., China) once daily. The MET group was intragastrically administered metformin (300 mg/kg body weight; Selleck Biotechnology Co., Ltd., USA) once daily.
4 (link) Pirfenidone and metformin were administered to the PFD + MET group. The DPI group was injected with DPI (1 mg/kg body weight; Santa Cruz Biotechnology Co., Ltd., USA) once daily. The control group and the BLM group were given the same volume of saline every day. The mice were sacrificed on Day 21, and the lungs were collected for histological staining, hydroxyproline (HPO) assays, and oxidation–reduction analysis.
Liu N., Song Y., Liu T., Wang H., Yu N, & Ma H. (2024). Metformin enhanced the effect of pirfenidone on pulmonary fibrosis in mice. The Clinical Respiratory Journal, 18(1), e13731.
Publication 2024
5
Evaluating Pirfenidone Therapy Outcomes
The time interval between the date of initiation of pirfenidone therapy and either day 28 after the last dose of pirfenidone (for those who prematurely discontinued treatment) [9 (link),43 (link)] or 30 September 2023 (for those who continued the treatment) was considered “on-treatment”. “High dose” and “low dose” referred to 1800 mg and 1200 mg of pirfenidone per day (in divided doses; these are the dosages approved by the Taiwan Food and Drug Administration), respectively [8 (link)]. “AE-IPF” was defined using previously published working definitions and specifically excluded events with identifiable infectious or non-infectious etiologies [5 (link)]. Patients who underwent lung transplantation or died from any cause while receiving pirfenidone (or within 28 days of the last dose) were defined as having had “severe adverse outcomes” (SAO). SAO that occurred within two years after pirfenidone treatment had begun were considered as “early SAO”. Pulmonary hypertension referred to an estimated systolic pulmonary arterial pressure (based on the tricuspid regurgitation jet velocity) of ≥35 mmHg, determined via transthoracic echocardiography [43 (link),45 (link)]. When determining the annualized (52-week) and 24 week rates of change in FVC and DLCO, we used the formulae presented in Appendix S1 of the Supplementary Materials.
Huang T.H., Wei S.H., Kuo H.I., Hou H.Y., Kuo C.W., Tseng Y.L., Lin S.H, & Wu C.L. (2024). Baseline Blood Levels of Mucin-1 Are Associated with Crucial On-Treatment Adverse Outcomes in Patients with Idiopathic Pulmonary Fibrosis Receiving Antifibrotic Pirfenidone. Biomedicines, 12(2), 402.
Publication 2024

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1
Pirfenidone by Selleck Chemicals
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Pirfenidone is a chemical compound used in laboratory settings. It serves as a key ingredient in various research and experimentation processes, though its core function is not subject to interpretation or extrapolation within this factual description.
2
Pirfenidone by Merck Group
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Pirfenidone is a laboratory reagent used in research and development applications. It is a small molecule compound that acts as a multifunctional signaling inhibitor. Pirfenidone can be used in cell culture and biochemical assays to investigate various biological processes.
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Nintedanib by Selleck Chemicals
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9
Dimethyl sulfoxide (dmso) by Merck Group
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
10
Penicillin by Thermo Fisher Scientific
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.

More about "Pirfenidone"

Pirfenidone is a small molecule drug used to treat idiopathic pulmonary fibrosis (IPF), a progressive and fatal lung disease characterized by scarring and stiffening of the lungs.
Also known as Esbriet, this medication works by reducing inflammation and slowing the progression of fibrosis in the lungs, helping to preserve lung function.
Researchers can optimize their Pirfenidone studies using PubCompare.ai, an AI-driven platform that identifies the best protocols from published literature, preprints, and patents.
By comparing various experimental approaches, PubCompare.ai enhances the reproducibility and accuracy of Pirfenidone research, ensuring scientists can find the most effective products and procedures.
This is crucial for advancing the understanding and treatment of IPF, a debilitating condition with no known cure.
In addition to Pirfenidone, related compounds and techniques like fetal bovine serum (FBS), TRIzol reagent, Prism 8 software, transforming growth factor beta-1 (TGF-β1), Nintedanib, RNeasy Mini Kit, dimethyl sulfoxide (DMSO), and penicillin may also be relevant for Pirfenidone studies.
Researchers can leverage the power of PubCompare.ai to optimize their investigations into these various aspects of IPF and Pirfenidone treatment, ultimately improving outcomes for patients suffering from this devastating lung disease.