The largest database of trusted experimental protocols
Protocol detail

Protocols for Determining Nutrient Digestibility

A standard digestibility study, in which the digestibility of a component in test feedstuff is determined, requires measuring the ingested amount of that component and the voided amount of given component of test feedstuff. The total collection and index methods have been widely used to determine the digestibility of components in swine and poultry diets. The total collection method requires an accurate measure of feed intake and fecal output for determining the amount of the component ingested and voided via feces, respectively. With these measurements, the digestibility of the component can be calculated as follows:
where Cinput and Coutput are the amount of component ingested and voided via the feces, respectively.
In a total collection study for swine, pigs are individually housed in crates and thereafter they are adapted to their crates and feed being given before fecal sample collection. The adaptation period usually lasts for 3 to 7 days before a collection period of 4 to 6 days (Adeola, 2001 ). During the adaptation period, a feeding level is adjusted to avoid feed refusal which results in additional work such as orts collection during the collection period as well as drying and analyzing the orts after the collection period. A level of feeding at 3 times maintenance (197 kcal/kg BW0.60; NRC, 2012 ) or approximately 3% to 4% of body weight (BW) per d is suggested as the sufficient level of feeding for the digestibility study with total collection method. During the collection period, colored markers such as ferric oxide, chromic oxide, and indigo carmine are commonly used for the identification of fecal output from a given ingested feed (Adeola, 2001 ; Kim et al., 2006 (link); Son et al., 2013 ). Once pigs are adjusted to the crates and feed, the collection period begins and ends with feeding the first and the last marked feed, respectively. In this period, the feces that voided between the first and second appearances of the marker are collected as the representative output that is associated with the fed quantities given in the collection period.
In a balance study, it is difficult to identify urine that belongs to specific feed because marker does not appear in the urine, thus the urine collection is generally conducted based on time. The quantitative urine collection starts from the day of the first marked feed offered and ends at the day of the last marked feed. With measurement of components in the urine, the metabolizability of the component can be calculated as follows:
where Curine is the amount of component voided via the urine.
In a digestibility study for poultry, the total collection method is not common for determining the fecal digestibility, because feces and urine are voided together in the form of excreta and it is difficult to separate the feces from the excreta and measure digestibility. There was an attempt to avoid this confounding effect of urine on the fecal digestibility using surgical technique such as colostomy (Okumura, 1976 (link)), however there are problems with the artificial anus including skin regrowth, intestinal stasis and hardening of fecal material (Paulson, 1969 ). Thus, the total collection method in poultry usually involves collecting excreta (feces+urine). Sibbald (1976) (link) developed the precision-fed rooster assay and McNab and Blair (1988) (link) later suggested some modification. In this assay, adult cockerels or roosters were fasted for 48 h prior to being fed test ingredients. During the fasting period, all birds are tube-fed 2 doses of 25 to 30 g of glucose (as an aqueous solution) at 8 and 32 h post-feed withdrawal, which partly alleviates the effects of starvation. At 48 h post-feed withdrawal, all birds are tube-fed 25 to 30 g of their assigned test ingredients that are in distilled water and ground through a 0.5 mm screen prior to feeding. Birds for determining endogenous losses are fed 50 g of glucose. The total collection of excreta is conducted for 48 h after feeding of test ingredients or glucose for endogenous losses determination. During 48-h collection period, all birds are given 50 ml of water by tube about 32 h after feeding to overcome any effects induced by low water intake.

Partial Protocol Preview
This section provides a glimpse into the protocol.
The remaining content is hidden due to licensing restrictions, but the full text is available at the following link: Access Free Full Text.

Publication 2014

Corresponding Organization : Purdue University West Lafayette

Protocol cited in 43 other protocols

1

FRET-based Enzymatic Inhibition Assay for SARS-CoV-2 3CL Protease

The FRET-based enzymatic inhibition assay was utilized to measure the inhibitory activities of compounds against 3CL proteases. Primary screening was carried out to identify the inhibitors against SARS-CoV-2 3CLpro using an FDA-approved drug library containing an array of 1,018 compounds obtained from Selleck Chemicals (#L1300) [30] (link). The fluorogenic substrate Dabcyl-KNSTLQSGLRKE-Edans (GenScript, Shanghai, China) was synthesized to measure the protease activity of SARS-CoV-2 3CLpro or SARS-CoV 3CLpro according to our previous method [30] (link), [37] (link). Dabcyl-KTSAVLQSGFRKME-Edans (GenScript, Shanghai, China) was used for enzymatic inhibition assay of MERS-CoV 3CLpro and HCoV-229E 3CLpro as described previously [38] (link), [39] (link). The enzymatic inhibition assays of different proteases were performed as follows. 120 nM of SARS-CoV-2 3CLpro in the reaction buffer (0.1 M PBS, 1 mM EDTA, pH 7.4) incubated with varying concentrations of tested compounds for 1 h at 37 °C and then the substrate (final concentration 20 μM) was added to start the reaction. Fluorescence intensity was monitored continuously every 2 min for up to 20 min with an excitation wavelength of 340 nm and emission wavelength of 490 nm by using Spectramax® ID3 plate reader (Molecular Devices, California, USA). For the SARS-CoV 3CLpro inhibition assay, 860 nM protease was mixed with 40 μM substrate in assay buffer.
To determine the effect of DTT or GSH on the enzymatic inhibition of SARS-CoV-2 3CLpro by Thonzonium bromide, we performed the enzymatic inhibition assay according to the literature [40] (link). SARS-CoV-2 3CLpro was preincubated in reaction buffer with Thonzonium bromide in the presence of 4 mM DTT or 1 mM GSH compared with in the absence of DTT or GSH buffer.
In the MERS-CoV 3CLpro and HCoV-229E 3CLpro enzymatic inhibition assay, the concentration of the proteases was 2 and 1 μM, corresponding to the final substrate concentration of 40 and 20 μM, respectively. The IC50 values were calculated by fitting the curve of normalized inhibition ratio with the different concentration of test compounds.
+ Open protocol
2

Measuring 3CLpro Protease Inhibition

For assessing the ability to inhibit the main protease (3CLpro), the IC50 was the half-maximal inhibitory concentration of the substance at which the fluorescence level reduced by 50% compared to the value obtained without adding the inhibitor [9 (link),10 (link),34 (link)]. Fluorescence occurred due to cleavage of the peptide substrate DabcylKTSAVLQ↓SGFRKME(Edans)NH2 by 3CLpro protease. ML188 inhibitor ((R)-N-(4-(tert-Butyl)phenyl)-N-(2-(tert-butylamino)-2-oxo-1-(pyridin-3-yl)ethyl)furan-2-carboxamide, Ambeed Inc, USA) was used as a positive control. In the study, the signal was recorded using the CLARIOstar Plus instrument (BMG Labtech) at 355 and 460 nm for excitation and radiation, respectively, in the kinetic scan mode. Reaction mixtures containing TrisHCl buffer, fluorogenic substrate, 3CLpro, and the compound being tested were prepared and incubated for 30 min in a 384-well plate at 30 °C. The measurement for each compound was carried out in triplicate. The instrument was calibrated using a solution of the peptide that had undergone complete hydrolysis. The accompanying MARS Data Analysis software was used to calculate IC50 values.
+ Open protocol
3

Inhibition of SARS-CoV-2 3CLpro Protease

To assess the ability to inhibit the main protease (3CLpro), the IC50 is the semi-inhibitory concentration of the substance, at which the fluorescence level is reduced by 50% relative to the value obtained without adding the inhibitor [30 (link)]. Fluorescence occurs due to cleavage of the peptide substrate DabcylKTSAVLQ↓SGFRKME(Edans)NH2 by 3CLpro protease. In the study, the signal was recorded using the CLARIOstar Plus instrument (BMG Labtech) at 355 and 460 nm for excitation/radiation, respectively, in kinetic scan mode. Reaction mixtures containing TrisHCl buffer, fluorogenic substrate, 3CLpro, and the compound being tested were prepared and incubated for 30 min in a 384-well plate at 30 °C. The instrument was calibrated using a solution of the peptide that had undergone complete hydrolysis. The accompanying MARS Data Analysis software (https://www.selectscience.net/products/mars-data-analysis-software/?prodID=81306, accessed on 18 August 2022) was used to calculate IC50.
+ Open protocol
4

Repurposing Drugs for COVID-19 Treatment

The first step involved the curation and preparation of the experimental screening data. We downloaded the data on SARS-CoV-2 cytopathic effect (CPE) from the NCATS COVID-19 portal. This assay measures the ability of a compound to reverse the cytopathic effect induced by the virus in Vero E6 host cells (one of the most commonly used cell lines for studying this family of virus). The assay provides valuable basic information about the ability of a compound to restore the cells’ function but does not provide indication of the possible mechanism of action(s) of the small chemical compound under study. We also explored using the same Vero E6 cells the cytotoxic effect of these molecules in a counterscreen since the observed effect of some compounds may be mediated through cell viability and could lead to erroneous interpretation of the CPE results. Such information on cell viability is evidently important in the applicability of such compounds in clinical pharmacological interventions. Some additional data are important to take into account in the present analysis and involve the effect of the chemical compounds on human fibroblasts. This assay measures the host cell ATP content as a readout for cytotoxicity. When available, we annotated further the CPE data with the results of this assay. To be able to quickly repurpose a compound, we focused essentially on molecules that have been approved or are in clinical trials (in some instances, drugs are only approved for veterinary use). We thus cross-linked the CPE sample ID numbers to drug names (eg, international nonproprietary names), PubChem SID or CID numbers23 (link) or to ChEMBL ID numbers24 (link) and to molecules that possess ATC (Anatomical Therapeutic Chemical Classification system) codes and/or have documented therapeutic indications as found in DrugBank,25 (link) DrugCentral26 (link) and eDrug3d.27 (link) Molecules that are at the preclinical stage (eg, chemical probes) were essentially excluded via this procedure. Additionally, the salts, when present in the chemical file, were deleted using the Maya chemistry toolkit,28 (link) and the chemistry of the molecules was standardized using our FAF-Drugs4 web server.29 (link) The drugs in duplicate were removed. Further curation of the CPE data also involved the following: i) removal of a few molecules without potency values (AC50 values are reported for this dataset, ie, concentration for half-maximal activity30 (link)), ii) investigation of the curve class (ie, the evaluation of the quality of the dose–response curve and thus the quality of the measurements) in the CPE data (a curve class of type 4 is a flat curve indicating no activity) and maximum response (ie, maximum response value detected in the experiment). In such assay, compounds are usually considered active when the maximum response (absolute) value is above 30.31 Further, we removed molecules that were found highly cytotoxic in the Vero E6 counterscreen assay. From the initial CPE data containing 10,721 assessed samples (some molecules have been screened several times and most are chemical probes), we ended up with a list of 198 bioactive drugs. In this list of drugs, 93 were not tested for toxicity on human fibroblast and for the remaining 105 molecules, only one was found cytotoxic (Disulfiram, used for alcohol addiction, this molecule was also removed not only because of its cytotoxic nature in these assays but also as found to be a promiscuous SARS-CoV–2 main protease inhibitor32 (link)). At this stage of the analysis, we decided to retain all the compounds including those not annotated for human fibroblast toxicity. We then focused our attention on families of molecules that contain several members and removed some molecules with highly specific disease indication such as Deferasirox (an oral iron chelator given to patients receiving long-term blood transfusions). In this last step of data curation, we grouped the 198 compounds according to chemistry and disease indications and removed molecules that did not fulfill our selection criteria. This step led to the selection of a final list of 161 molecules reported in Table 1. Numerous approaches can be used to investigate low molecular weight chemical compounds in silico (eg,33–35 (link)) and here we decided to analyze these molecules with DataWarrior.36 (link) In this final list, very few molecules are only chemical probes, like Calpeptin (moderate activity against SARS-CoV-2 main protease Mpro). They were kept because they are often used to assess some enzymatic activities. The structural classification of chemical entities was then performed using the ClassyFire application.37 (link)

Investigated Chemical Probes and Approved Drugs

NameIndicationAC50 (uM)Fibroblast-ToxicityClinicalTrials.gov (Feb 24, 2021)cLogPSimple Rule-Based Estimation of Basic Nitrogen Atoms
AbemaciclibCancer1.412537545Not determined (ND)No4.11544
AcetopromazinePsychotropic12.58925412No (N)No3.87211
AcolbifeneCancer11.22018454NDNo4.98461
AmiodaroneCardiovascular8.912509381NYes6.28011
AmitriptylinePsychotropic12.58925412NNo4.40561
AmlodipineCardiovascular12.58925412NDYes2.0711
AmodiaquineInfectious1.584893193NDYes4.20182
AmoxapinePsychotropic8.912509381NNo3.30352
AndrographolideInfectious11.22018454NDNo1.8830
AnidulafunginInfectious5.623413252NDNo−0.49510
ApilimodInfectious12.58925412NDYes5.19422
AprindineCardiovascular8.912509381NNo4.50091
Arbidol (or Umifenovir)Infectious8.912509381NDYes4.16891
AripiprazolePsychotropic12.58925412NNo4.43511
AsenapinePsychotropic10NDNo4.94051
Ataciguat (experimental)Cardiovascular12.58925412NDNo1.80360
AzelastineAntihistamine11.22018454NNo4.37441
AzithromycinInfectious11.22018454NYes1.65692
BazedoxifeneBone problems and possibly Cancer3.981071706NNo5.69681
BenazeprilCardiovascular10NYes0.87151
BencyclaneCardiovascular12.58925412NNo3.86391
BepridilCardiovascular8.912509381NNo4.40441
Berbamine (experimental)Cancer1.412537545NDNo6.22532
Berzosertib (experimental)Cancer2.238721139NDNo1.6691
BexaroteneCancer12.58925412NNo4.7990
Bifemelane (approved Japan)Psychotropic12.58925412NNo3.74761
Blonanserin (Japan)Psychotropic5.623413252NNo5.36822
BrexpiprazolePsychotropic11.22018454NDNo3.89831
BromodiphenhydramineAntihistamine12.58925412NNo3.6311
BuclizineAntihistamine12.58925412NNo6.68272
Calpeptin (experimental)Cancer0.316227766NDNo2.83580
CarvedilolCardiovascular11.22018454NDYes3.16681
CenicrivirocInfectious8.912509381NDYes7.26061
CeritinibCancer10NDNo5.58173
ChlorcyclizineAntihistamine12.58925412NNo3.68272
ChloroquineInfectious3.981071706NYes4.00912
ChloroxineInfectious12.58925412NNo2.84190
ChlorpromazinePsychotropic8.912509381NYes4.60691
ChlorprothixenePsychotropic3.548133892NNo5.12161
CiclopiroxInfectious5.011872336NNo1.42850
CilnidipineCardiovascular11.22018454NNo3.64090
ClemastineAntihistamine11.22018454NNo4.59881
Clioquinol (withdrawn)Infectious10NNo2.6730
ClofazimineInfectious6.309573445NDYes6.27811
ClomipraminePsychotropic7.943282347NNo4.49691
Closantel (veterinary drug, likely toxic in humans)Infectious11.22018454NNo6.42420
ClozapinePsychotropic12.58925412NNo3.24472
CyclobenzaprineInitially used as Psychotropic10NNo4.35341
CyproheptadineAntihistamine3.981071706NNo4.59991
Cysmethynil (experimental)Cancer10NDNo5.90270
DabrafenibCancer12.58925412NDNo3.6660
DanazolCancer and endometriosis12.58925412NNo3.46380
DapoxetineInitially psychotropic agent but now premature ejaculation12.58925412NNo4.23671
DeserpidineCardiovascular12.58925412NDNo3.64541
DesipraminePsychotropic8.912509381NNo3.62441
DesloratadineAntihistamine11.22018454NNo4.05831
Desmethylclozapine (metabolite of clozapine)Psychotropic8.912509381NDNo2.99182
Dexanabinol (experimental)Cancer10NDNo6.93550
DifeterolAntihistamine12.58925412NNo4.04321
Doramectin (veterinary drug)Infectious12.58925412NDNo5.35160
DosulepinPsychotropic12.58925412NDNo3.82011
DoxazosinCancer and hypertension12.58925412NYes2.13792
DuloxetinePsychotropic8.912509381NNo3.83681
EfavirenzInfectious10NNo3.66140
Emodepside (veterinary drug)Infectious7.079457844NDNo5.2370
Enzastaurin (experimental)Cancer12.58925412NNo3.10991
Flumatinib (experimental)Cancer7.943282347NDNo3.83972
FlunarizineAntihistamine11.22018454NNo5.45762
FluoxetinePsychotropic4.466835922NYes3.62411
Fluphenazine-decanoatePsychotropic12.58925412NNo8.5272
Fonazine (Japan and Europe)Antihistamine28.18382931NDNo3.12441
HalofantrineInfectious11.22018454NNo8.17621
HaloperidolPsychotropic25.11886432NNo4.30491
Hesperadin (experimental)Cancer12.58925412NDNo2.37681
HexachloropheneInfectious0.223872114NNo6.42010
HexetidineInfectious3.548133892NNo5.25871
Homochlorcyclizine (Japan)Antihistamine5.011872336NNo4.02472
HycanthoneInfectious12.58925412NDNo3.32121
HydroquinidineCardiovascular12.58925412NDNo2.79591
IcaritinCancer12.58925412NDNo4.13410
IloperidonePsychotropic12.58925412NNo4.30441
ImatinibCancer5.623413252NYes3.93832
ImipraminePsychotropic8.912509381NNo3.89091
LapatinibCancer10NNo4.72811
Lemildipine (experimental)Cardiovascular12.58925412NNo3.38870
LercanidipineCardiovascular11.22018454NNo4.71021
LetermovirInfectious10NDNo4.86151
LomerizineAntihistamine (treatment of migraines)12.58925412NNo4.48642
LopinavirInfectious12.58925412NYes4.8470
LoratadineAntihistamine10NNo4.97740
LoxapinePsychotropic10NNo3.55641
Manassantin-A (experimental)Cancer3.16227766NDNo5.83180
ManidipineCardiovascular8.912509381NNo2.61322
MaprotilinePsychotropic8.912509381NNo3.70291
MasitinibCancer11.22018454NDYes4.75733
MefloquineInfectious11.22018454NDYes3.50761
MelitracenPsychotropic11.22018454NDNo4.66471
MerimepodibInfectious12.58925412NDYes2.71960
MesoridazinePsychotropic10NNo4.55791
MethdilazineAntihistamine7.079457844NDNo4.20051
MethotrimeprazinePsychotropic12.58925412NDNo4.14921
Momelotinib (experimental)Cancer12.58925412NDNo2.50620
Monatepil (experimental)Cardiovascular12.58925412NNo4.72691
NafronylPsychotropic12.58925412NDNo4.29811
NaftopidilCancer12.58925412NNo3.421
NicardipineCardiovascular10NNo1.55821
NiraparibCancer12.58925412NDNo2.06191
NirogacestatCancer12.58925412NDNo4.36313
NitazoxanideInfectious3.16227766NYes1.68710
NitroxolineInfectious12.58925412NDNo0.70830
OxatomideAntihistamine10NNo4.27612
PamelorPsychotropic12.58925412NDNo4.13911
ParthenolideCancer10NDNo2.75250
PazopanibCancer12.58925412NDNo0.91252
PericiazinePsychotropic10NDNo4.11741
PerphenazineAntihistamine and psychotropic12.58925412NNo4.16492
Pipequaline (experimental)Psychotropic12.58925412NDNo4.97631
Piperacetazine (prodrug)Psychotropic12.58925412NNo4.80211
Piroctone (experimental)Infectious and Cancer7.943282347NDNo2.90440
PizotifenPsychotropic and antihistamine10NNo4.51871
Pluripotin (experimental)Cancer12.58925412NDNo4.28740
ProchlorperazinePsychotropic8.912509381NNo4.68532
PromazinePsychotropic10NNo4.00091
PromethazineAntihistamine8.912509381NYes3.90581
PropafenoneCardiovascular12.58925412NNo3.08371
Propionylpromazine (veterinary drug)Antihistamine and neuroleptic10NNo4.32651
ProtriptylinePsychotropic12.58925412NNo3.68481
PyrimethamineInfectious4.466835922NDNo2.54142
QuinidineCardiovascular12.58925412NDNo2.61041
Quizartinib (experimental)Cancer2.511886432NDNo4.79792
Refametinib (experimental)Cancer11.22018454NDNo1.880
RemdesivirInfectious7.943282347NDYes0.30480
Rescimetol (Japan)Cardiovascular12.58925412NNo3.69891
ReserpineCardiovascular11.22018454NYes3.57541
RetapamulinInfectious12.58925412NDNo5.2181
SarpogrelateCardiovascular12.58925412NNo1.85671
Serdemetan (experimental)Cancer8.912509381NDNo3.72371
Siccanin (experimental)Infectious12.58925412NDNo4.36370
Spiclomazine (experimental)Cancer12.58925412NDNo5.21691
Spiperone (Japan)Psychotropic7.943282347NNo3.02191
Spiramycin-IIInfectious12.58925412NNo2.46082
Sulfatinib (experimental)Cancer12.58925412NDNo2.09181
TeicoplaninInfectious14.12537545NDYes−3.41941
ThioproperazinePsychotropic11.22018454NNo3.29792
ThiothixenePsychotropic12.58925412NDNo2.9372
TiloroneInfectious10NDNo4.06072
Timiperone (Japan)Psychotropic10NDNo3.74071
TioguanineCancer10NDNo−0.96831
Tipifarnib (experimental)Cancer12.58925412NDNo4.032
Tivantinib (experimental)Cancer12.58925412NDNo4.18370
TizoxanideInfectious3.16227766NDYes1.35470
TriamtereneCardiovascular7.079457844NYes0.60752
TrifluomeprazinePsychotropic10NDNo5.06751
TrifluoperazinePsychotropic12.58925412NDNo4.92762
TriflupromazinePsychotropic11.22018454NNo4.84921
Trimeprazine (or Alimemazine)Psychotropic8.912509381NNo4.21921
TrimetrexateCancer10NDNo1.97862
TrimipraminePsychotropic10NNo4.10921
VilazodonePsychotropic10NDNo3.66291
VorapaxarCardiovascular8.912509381NDNo4.78650
ZotepinePsychotropic12.58925412NNo4.67411

Notes: The names of the 161 selected bioactive molecules are reported in the first column. For each compound, the main indication, the experimental AC50 values (see text), the experimental fibroblast toxicity (ND, not determined, N, No), the computed log P (cLogP), and a simple estimation of the number of basic nitrogen atoms are shown. Also, molecules that are in clinical trials for COVID-19 treatments indicated; Experimental and investigational drugs are all labelled in this Table experimental.

+ Open protocol
5

Fluorescence Polarization Assay for Mpro Inhibitor Screening

In this FP screening assay, 29 µL sample of 400 nM Mpro diluted in the FP assay buffer was mixed with 1 µL of natural product (1 mg/mL in DMSO) in a black 384-well microplate, and the mixture was further incubated for 35 min at RT before adding 20 µL sample of 60 nM FP tracer. After proceeding for 20 min at RT, the reaction was quenched by addition of 10 µL sample of 300 nM avidin, and the mP values were measured by a microplate reader. In each assay plate, GC-376 (1 µM) and DMSO were used as a positive and negative control, respectively. The well containing only 60 µL sample of 20 nM FITC-AVLQ peptide was used to assess the background noise. The inhibitory activity of screening compound was calculated using Eq. (1), and the candidate compounds (> 50% inhibition) were analyzed in triplicate to generate the dose-response curves in the second screening.
The inhibitory activity of dieckol in this FP screening assay was carried out as mentioned above. The initial concentration of dieckol was 100 µM, and 8 two-fold dilutions were prepared for the determination of IC50 value. To remove the DTT effect on the enzymatic assay [26 (link)], the IC50 value was also obtained in the absence of DTT in a FP screening assay.
+ Open protocol

Variable analysis

independent variables
  • Feeding level (3 times maintenance, approximately 3% to 4% of body weight per day)
dependent variables
  • Digestibility of a component in test feedstuff
  • Metabolizability of the component
control variables
  • Adaptation period (3 to 7 days) before collection period (4 to 6 days)
  • Use of colored markers (ferric oxide, chromic oxide, indigo carmine) for identification of fecal output
positive controls
  • Feeding 50 g of glucose for determining endogenous losses in precision-fed rooster assay
negative controls
  • No negative controls explicitly mentioned

Annotations

Based on most similar protocols

Etiam vel ipsum. Morbi facilisis vestibulum nisl. Praesent cursus laoreet felis. Integer adipiscing pretium orci. Nulla facilisi. Quisque posuere bibendum purus. Nulla quam mauris, cursus eget, convallis ac, molestie non, enim. Aliquam congue. Quisque sagittis nonummy sapien. Proin molestie sem vitae urna. Maecenas lorem.
Sign up for free or login to display all annotations

As authors may omit details in methods from publication, our AI will look for missing critical information across the 5 most similar protocols.

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required

Sign up now

Revolutionizing how scientists
search and build protocols!