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Cytostatic Agents

Q: What are the key considerations when using Cytostatic Agents in cancer treatment?

Cytostatic Agents are potent anti-cancer drugs that work by disrupting the cell cycle and selectively eliminating rapidly dividing tumor cells. Key considerations when using these agents include careful dosing to minimize harm to healthy tissues, monitoring for potential side effects, and integrating them into a comprehensive cancer treatment regimen along with other therapies. Proper protocl selection and optimization is crucial for maximizing the effectiveness of Cytostatic Agents.

Q: How can researchers identify the most effective protocols for using Cytostatic Agents?

PubCompare.ai's AI-driven platform can greatly assist researchers in optimizing protocols for Cytostatic Agents. The tool allows you to efficiently screen the literatrue to identify the most reproducible and accruate protocols. Its AI analysis can highlight key differences in protocol effetiveness, enabling you to choose the best option for your specific research goals. This helps ensure you're leveraging the most effective Cytostatic Agent protocols to enhance your cancer research.

Q: What are some common variations or types of Cytostatic Agents?

Cytostatic Agents encompass a diverse range of pharmaceutical compounds that target different stages of the cell cycle. Common types include antimetabolites that disrupt DNA synthesis, mitotic spindle poisons that interfere with cell division, and topoisomerase inhibitors that prevent DNA unwinding. Each class of Cytostatic Agent has unique mechanisms of action and is suited for different cancer types and treatment contexts. Carefully selecting the right Cytostatic Agent variation is key for optimizing anti-tumor efficacy.

Cytostatic Agents are a class of pharmaceutical compounds that inhibit or prevent cell growth and division.
They are commonly used in the treatment of cancer, acting to disrupt the cell cycle and induce cell death in rapidly dividing tumor cells.
These agents may target specific stages of the cell cycle, such as DNA synthesis or mitosis, to selectively eliminate cancerous cells while minimizing harm to healthy, non-dividing tissues.
Cytostatic Agents play a crucial role in modern oncology, offering potent anti-tumor activity when used as part of comprehensive cancer treatment regimens.
Reserachers can leverage PubCompare.ai's AI-driven platform to optimzie research protocols for Cytostatic Agents, effortlessly locating and comparing the most reproducible and accurate protocols and products from the literature, preprints, and patents.

Most cited protocols related to «Cytostatic Agents»

Modeling Cell Growth Dynamics Under Drug Response

To simulate the effect of division time on GR and conventional drug response metrics under different assumptions about the degree of cytostasis or cell killing, we developed a theoretical model of drug response. To the first approximation, cell growth can be considered exponential, with drugs either decreasing the division rate or killing cells in a cell cycle-dependent manner:

ẋ = x \cdot k (1 - \frac{S_{M} \cdot c^{h}}{S C_{50}^{h} + c^{h}}),

where x is the cell count, k is the untreated growth rate (per day), c is the drug concentration, S_M is the maximal inhibitory effect, SC₅₀ is the concentration at half-maximal effect of drug, and h the Hill coefficient. The growth rate k corresponds to the division rate k₀ as k = ln(2)·k₀ = ln(2)/T_d, where T_d is the division time. S_M can be larger than 1 to account for drugs inducing cell death at a specific phase of the cell cycle. The model can also be generalized to account for drugs that induce cell death independent of the cell cycle:

ẋ = x \cdot k (1 - \frac{S_{M} \cdot c^{h}}{S C_{50}^{h} + c^{h}}) - x \cdot (\frac{k_{L} \cdot c^{h}}{L C_{50}^{h} + c^{h}}),

where k_L is the maximal killing rate (per day), LC₅₀ is the concentration of drug that produces half-maximal cell killing. Integrating these equations for an assay of t days yields the cell count at concentration c:

x (c, t) = x_{0} \cdot exp (t \cdot k (1 - \frac{S_{M} \cdot c^{h}}{S C_{50}^{h} + c^{h}}) - t \frac{k_{L} \cdot c^{h}}{L C_{50}^{h} + c^{h}}),

where x₀ ≡ x(t = 0) is the cell number at the time of treatment. Thus, the relative cell count is:

I C (c, t) = \frac{x (c, t)}{x_{ctrl}} = exp (- t \cdot k \frac{S_{M} \cdot c^{h}}{S C_{50}^{h} + c^{h}} - t \frac{k_{L} \cdot c^{h}}{L C_{50}^{h} + c^{h}}) where x_{ctrl} \equiv x (0, t),

and the normalized growth rate inhibition (GR value) is:

G R (c, t) = 2^(\frac{{log}_{2} (\frac{x (c, t)}{x_{0}})}{{log}_{2} (\frac{x_{ctrl}}{x_{0}})}) - 1 = 2^(1 - \frac{S_{M} \cdot c^{h}}{S C_{50}^{h} + c^{h}} - \frac{1}{k} \cdot \frac{k_{L} \cdot c^{h}}{L C_{50}^{h} + c^{h}}) - 1 .

This equation for GR(c) is independent of the length of the assay t and thus, the metrics GR₅₀, GR_max, GR_AUC, and h_GR are also independent of t. For cases where drug action is mainly related to the cell cycle (k_L =0), GR values are also independent of the untreated growth rate k. As shown in Supplementary Fig. 2 and 3a–b, the impact of k_L>0 is minimal on GR₅₀ and relatively small on GR_max. This is also illustrated by the analytical formula for GR_inf·GR_inf = 2^(1 − S_M − k_L/k) − 1. Note that the metrics derived from growth inhibition (GI) values used in Heiser et al.^{3 (link)} such as GI₅₀ are more robust than traditional metrics, but still depend on both division time and assay length (see Supplementary Note).

Hafner M., Niepel M., Chung M, & Sorger P.K. (2016). Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. Nature methods, 13(6), 521-527.

Publication 2016

Biological Assay Cell Cycle Cytostatic Agents Pharmaceutical Preparations Psychological Inhibition

Phase II Cancer Clinical Trial Design

For ease of exposition, our methodology will be developed in the context of phase II cancer clinical trials. In this setting, many drugs have been evaluated with tumor response, which has a specific definition that loosely translates into a reduction in the tumor size (or reduction in overall volume of disease).^{14 (link)} The probability of response will be designated with π_r. Another variable of interest in phase II oncology is the probability a patient survives without experiencing a progression of disease for a specified period of time (say 6 months or 2 years, depending on the aggressiveness of the disease). We will use 6 months as a matter of convenience and denote this binomial variable as “6-month progression-free survival (PFS)” or “at risk for PFS at 6 months.” The probability of this event will be designated with π_s. Tumor response is a variable that is capable of detecting agents that are effective at selectively killing tumor cells (cytotoxic) whereas 6-month PFS is capable of detecting agents that can stabilize disease but are not necessarily effective at cell kill (cytostatic).
The null hypothesis is formulated as follows: H₀ : π_r ≤ π_r0, and π_s ≤ π_s0, where π_r0 and π_s0 are specified values (obtained from historical data) that are believed to be uninteresting or comparable to the current standard of care. The alternative hypothesis is the complement of this null parameter space. Commonly the area of the parameter space where high statistical power is desired can be written as follows: H₁ : π_r ≥ π_r1 = π_r0 + Δ_ror π_s ≥ π_s1 = π_s0 + Δ_s where Δ_r and Δ_s are the (minimal) clinically significant improvements in the proportion responding and with 6-month PFS, respectively.

Sill M.W., Rubinstein L., Litwin S, & Yothers G. (2012). A Method for Utilizing Bivariate Efficacy Outcome Measures to Screen Regimens for Activity in 2-Stage Phase II Clinical Trials. Clinical trials (London, England), 9(4), 385-395.

Publication 2012

Cells Cytostatic Agents Disease Progression Malignant Neoplasms Neoplasms Patients Pharmaceutical Preparations

Fitting Growth Regulatory Curves

GR data are fitted to a sigmoidal curve as follows (Supplementary Fig. 8a–c):

G R (c) = G R_{inf} + \frac{1 - G R_{inf}}{1 + {(c / G E C_{50})}^{h_{G R}}}

where the fitted parameters are:

GR_inf: the effect of the drug at infinite concentration (GR_inf ≡ GR(c → ∞)). GR_inf lies between −1 and 1; negative values correspond to cytotoxic responses (i.e. induction of cell death, Supplementary Fig. 8a), a value of 0 corresponds to a fully cytostatic response (Supplementary Fig. 8b), and a positive value to partial growth inhibition (Supplementary Fig. 8c).

h_GR: the Hill coefficient of the fitted curve which reflects how steep the dose response curve is. In practice, we typically constrain h_GR to a value between 0.1 and 5.

GEC₅₀: the concentration at half-maximal effect. To avoid artefacts in curve fitting we constrain GEC₅₀ to be two orders of magnitude higher and lower than the experimentally tested concentration range (in practice, this is usually about 10⁻⁷ to 10³ µM).

If the fit of the curve is not significantly better than that of a flat curve (i.e. GR(c) ≡ GR_inf) based on an F-test with cutoff of p = 0.05, the response is considered flat and the parameter GEC₅₀ is set to 0 (Supplementary Fig. 8d).

Hafner M., Niepel M., Chung M, & Sorger P.K. (2016). Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. Nature methods, 13(6), 521-527.

Publication 2016

Cell Death Cytostatic Agents Psychological Inhibition STEEP1 protein, human

Antimalarial Drug Potency Assay

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Publication 2011

Amodiaquine Biological Assay Cells chloroquine phosphate Cytostatic Agents Ethanol Fluorescence Medical Devices Mefloquine Hydrochloride Parasite Control Parasitemia Parasites Pellets, Drug Pets Pharmaceutical Preparations Primaquine Diphosphate Protoplasm Quinidine Quinine SYBR Green I Technique, Dilution Verapamil Hydrochloride Volumes, Packed Erythrocyte

Serum Creatinine Reference Ranges in Healthy Children

In order to include measurements of children with normal serum creatinine level only, several steps of exclusion were carried out. Firstly, to prevent the influence of serial measurements, we randomly selected one assay per patient. Secondly, all determinations requested by the departments of Paediatric Nephrology, Paediatric Oncology and the Neonatal and Paediatric Intensive Care Units were excluded. Thirdly, the remaining patients were screened for pathophysiological conditions that could cause renal damage (Table 2).
Table 2

Exclusion criteria and the method of exclusion

Exclusion criterion	Method of exclusion	n^a
Kidney disease	Exclude all cases with kidney disease described in medical record	62
Use of cytostatic drugs	Exclude all patients receiving cytostatic drugs or with proven malignancy described in medical record	12
Premature	Exclude all patients with gestational age <37 weeks described in medical record	224
Small for gestational age	Exclude all cases if birth weight was: - <2300 g if gestational age = 37 weeks - <2500 g if gestational age = 38 weeks - <2700 g if gestational age = 39 weeks - <2900 g if gestational age = 40 weeks - <3000 g if gestational age = 41 weeks - < 3100 g if gestational age = 42 weeks	64
Muscle disease	Exclude all patients with muscle disease described in medical record	1
Haemolysis	Exclude all patients with proven haemolysis described in medical record or found in laboratory tests	0
Hyperbilirubinaemia	Exclude all patients with hyperbilirubinaemia proven with laboratory test	32
Hypertriglyceridaemia	Exclude all patients with hypertriglyceridaemia proven with laboratory test	2
Syndromes	Exclude all patients with a syndrome described in medical record. Exclude all patients with multiple congenital dysmorphisms described in medical record	79
After major surgery	Exclude all determinations performed after (cardio)thoracic surgery or extensive abdominal surgical procedure described in medical record	128
Prerenal problems	Exclude all patients with shock, dehydration, heart failure or cardiopulmonary resuscitation described in medical record	131
Urological problems	Exclude all patients with hydronephrosis, vesicoureteral reflux, urinary tract infection described in medical record	128

^aThe total number of exclusions is >748 because some patients were excluded for more than one reason

Patients born preterm (<37 weeks of gestational age) or small for gestational age (birth weight <10th percentile according to The Netherlands Perinatal Registry 2007 [13 ]) were excluded because of their expected immature renal function. All patients with a proven or suspected syndrome were also excluded, for many syndromes are associated with multiple organ anomalies, including renal pathology. Finally, during measurement on the Hitachi 912, those indices possibly associated with interference with the enzymatic method (hyperbilirubinaemia, hypertriglyceridaemia and haemolysis) were measured in each sample. Samples with indications of haemolysis, hyperbilirubinaemia or hypertriglyceridaemia were excluded. All patients with muscle disease were also excluded.
All assay results from 1- to 7-day-old children were included in view of the expected rapid initial decline in serum creatinine during the first days of life. For older children up to 3 months of age, 15 random determinations per week were included; for those between 3 and 12 months, five random determinations per week.
The exclusion procedure was carried out by two physicians who were blinded to the serum creatinine levels.

Boer D.P., de Rijke Y.B., Hop W.C., Cransberg K, & Dorresteijn E.M. (2010). Reference values for serum creatinine in children younger than 1 year of age. Pediatric Nephrology (Berlin, Germany), 25(10), 2107-2113.

Publication 2010

Abdomen Biological Assay Birth Weight Cardiopulmonary Resuscitation Child Childbirth Congestive Heart Failure Creatinine Cytostatic Agents Dehydration Enzymes Gestational Age Hemolysis Hydronephrosis Hyperbilirubinemia Hypertriglyceridemia Infant, Newborn Kidney Kidney Diseases Malignant Neoplasms MLL protein, human Multiple Abnormalities Myopathy Neoplasms Operative Surgical Procedures Patients Physicians Pregnancy Serum Shock Syndrome Thoracic Surgical Procedures Urinary Tract Infection Vesico-Ureteral Reflux

Most recents protocols related to «Cytostatic Agents»

Comprehensive Genotoxicity Evaluation of PBMCs

After overnight fasting, 16 mL of venous blood samples have been collected from the participants in the morning using EDTA tubes (Greiner Bio-One, Kremsmunster Austria). For the isolation of peripheral blood mononuclear cells (PBMCs), Ficoll density graduation was applied using Ficoll separation tubes (Greiner Bio-One). The protocol of Fenech et al. [15 (link)] was applied to conduct the cytokinesis block micronucleus cytome (CBMN) assay as described previously [[48] (link), [49] (link), [50] (link), [51] (link)]. For stimulating the PBMCs into mitotic cell division, a concentration of 1 × 10⁶ cells/mL in culture medium were treated with phytohaemagglutinine (PHA-Sigma- Aldrich). The PBMC samples were incubated at 37 °C and 5% CO₂ for 72 h. After 44 h of incubation cytochalasin B (Sigma Aldrich, Vienna, Austria) was added in order to stop cell division. In the next step, the cells were loaded on microscope slides using a Cytospin (Thermofisher Scientific) and stained using Diff-Quick (Medion Diagnostics, Dudingen, Switzerland). A bright field microscope (1000- fold magnification; Olympus, Vienna, Austria) was used for counting the cells. It should be noted that duplicates of each PBMC sample were produced twice resulting in four slides per sample. In total 2000 cells per participant were counted. In order to reduce scorer bias and to decrease experimental variation, 500 cells of each slide were scored by two different scorers that were also recalibrating scoring accuracy regularly with standardized slides. For evaluating chromosomal stability of the PBMCs for each participant, MNi frequency was counted. Further, not only nucleoplasmic buds and bridges were scored but also the number of necrotic and apoptotic cells in total of 2000 binucleated cells. Additionally, the nuclear division index was calculated according to Fenech et al., to be able to assess mitogenic response and cytostatic effects of the PBMCs. The scoring was conducted by three different scorers to be able to manage counting the high number of CBMN microscopic slides of the study.

Draxler A., Franzke B., Kelecevic S., Maier A., Pantic J., Srienc S., Cellnigg K., Solomon S.M., Zötsch C., Aschauer R., Unterberger S., Zöhrer P.A., Bragagna L., Strasser E.M., Wessner B, & Wagner K.H. (2023). The influence of vitamin D supplementation and strength training on health biomarkers and chromosomal damage in community-dwelling older adults. Redox Biology, 61, 102640.

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Publication 2023

Apoptosis Biological Assay BLOOD Cells Chromosome Stability Culture Media cytochalasin H Cytokinesis Cytostatic Agents Diagnosis Division, Cell Edetic Acid Ficoll isolation Microscopy Mitogens Necrosis Nuclear Division PBMC Peripheral Blood Mononuclear Cells Veins

Preparation and Characterization of Pine WSPM

Preparation of pine WSPM,^{6 (link)} and the sources and properties of the DEP^{4 (link),5 (link)} and CFA^{3 (link)} have been described. Briefly, WSPM was prepared by burning

approximately 10 grams

of Austrian pine (from a tree growing in the Salt Lake Valley;

1.5 cm long multiply 0.2 to 0.5 cm wide

) using a pipe furnace at 750°C with constant air flow. WSPM was collected using an Anderson cascade impactor operated at

1 liter per minute

, and fractions 6 and 7 (

0.65 to 1.1 micrometers

and

0.43 to 0.65 micrometers

) were used. For experiments, WSPM concentrate was suspended in DMSO at

115 milligrams per milliliter

and diluted to

0.076 milligram per milliliter

in media containing

less than or equal to 0.2 percent

DMSO to achieve a

20 microgram per centimeter squared

area dose in a single well of a 6-well plate. Features of pine WSPM, and the effects that it has on AECs (i.e., calcium flux, pro-inflammatory, cytostatic, and cytotoxic) have been described.^{24 (link),25 (link),30 (link),31 (link)} Specifically, the material was shown to contain TRPA1 agonists, including resin acids, perinaphthenone, coniferaldehyde, ethyl phenols, and substituted xylenols; ethyl phenols and xylenols also activate TRPV3.^{6 (link),30 (link)} The DEP was collected from idling diesel-powered vehicles during emissions testing in the Salt Lake City area.^{4 (link)} The PM was suspended in media containing

less than or equal to 0.2 percent

DMSO and applied to cells at a final area dose of

10 micrograms per centimeter squared

. The DEP used in this study was shown to contain the TRPA1 agonists 2,4-di-tert-butylphenol (also a TRPV3 agonist) and several quinones (benzo and naptho), as well as perinanpthenone.^{4 (link)} Finally, CFA was collected from the Hunter power plant in Castle Dale, Utah, and fractionated to

less than 10 micrometers

. The ash was from low-sulfur bituminous coal, which was previously reported to consist of primarily insoluble oxides and salts of silicon, calcium, aluminum, and iron, with

approximately 3 percent

elemental carbon and

approximately 1 percent

unspecified organic carbon^{32 (link)} (presumably polycyclic aromatic hydrocarbons as described for other CFA samples^{33 (link)}). Effects of CFA on AECs and TRP channels have also been described.^{3 (link),26 (link),34 (link)}

Rapp E., Lu Z., Sun L., Serna S.N., Almestica-Roberts M., Burrell K.L., Nguyen N.D., Deering-Rice C.E, & Reilly C.A. (2023). Mechanisms and Consequences of Variable TRPA1 Expression by Airway Epithelial Cells: Effects of TRPV1 Genotype and Environmental Agonists on Cellular Responses to Pollutants in Vitro and Asthma. Environmental Health Perspectives, 131(2), 027009.

Publication 2023

Acids agonists Aluminum Bituminous Coal butylphen Calcium, Dietary Carbon Cells coniferaldehyde Cytostatic Agents Hay-Wells syndrome Inflammation Iron Oxides phenalen-1-one Phenols Pinus Polycyclic Hydrocarbons, Aromatic Quinones Resins, Plant Salts Silicon Sulfoxide, Dimethyl Sulfur Trees

Evaluating GBM Cell Invasiveness

A modified Boyden chamber technique (Greiner Bio-One, Kremsmünster, Austria) with Matrigel-coated membranes (Corning, Amsterdam, Netherlands) was used to examine the invasive behavior of GBM cells after treatment. Before seeding, cells were cultured for 24 h in a serum-free medium. After that, cells were seeded with serum-free medium supplemented with the cytostatic agents in the Matrigel-coated inserts (ThinCerts, 8 µm, Greiner Bio-One). To stimulate the cells to migrate through the membrane, the chamber below was filled with full medium. After 72 h, invading cells were quantified by WST-1 staining (1:10 in serum-free medium, Merck KGaA, Darmstadt, Germany). The analysis was done after 3 h incubation using the Tecan Reader at an excitation/emission of 480/650 nm. To document the invasiveness of tumor spheroids after treatment, 96-ULA well plates (Greiner Bio-One, Kremsmünster, Austria) were placed on ice after 4 days of sphere formation; half of the medium was removed, and cytostatic drugs were added including EGF (1%, ImmunoTools, Friesoythe, Germany) to stimulate the invasion into U-bottom wells containing ice-cold matrigel (Corning, Amsterdam, The Netherlands). The spheroids were monitored for 10 days and images were taken on days 0, 5, and 10 using the Leica microscope DMI 4000B (Leica, Heidelberg, Germany).

Linke C., Freitag T., Riess C., Scheffler J.V., del Moral K., Schoenwaelder N., Fiedler T., Fiebig A., Kaps P., Dubinski D., Schneider B., Bergmann W., Classen C.F, & Maletzki C. (2023). The addition of arginine deiminase potentiates Mithramycin A-induced cell death in patient-derived glioblastoma cells via ATF4 and cytochrome C. Cancer Cell International, 23, 38.

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Publication 2023

Cells Common Cold Cytostatic Agents matrigel Microscopy Neoplasm Invasiveness Serum Tissue, Membrane

Cytostatic Effect Evaluation Protocol

Cells were distributed into 96-well tissue culture plates with an initial cell number of 5.0 × 10³ per well. After 24 h incubation at 37 °C, the cells were treated with the compounds in 200 µL final volume containing 1.0 v/v% DMSO and 10% H₂O. The cells were incubated with the compounds at 3.125–25 µM concentration range for 24 h, whereas control cells were treated with serum-free medium only or with DMSO (c = 1.0 v/v%) and H₂O (c = 10.0 v/v%) at 37 °C for 24 h. After incubation, the cells were washed twice with a serum-free medium. To determine the in vitro cytostatic effect, the cells were further cultured up to 72 h in a 10% serum-containing medium. A solution of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and MTT-solution, (45 µL, 2 mg/mL, final concentration: 0.37 µg/mL) were added to each well. The respiratory chain [67 (link)] and other electron transport systems [68 (link)] reduce MTT, and thereby form non-water-soluble violet formazan crystals within the cell [69 (link)]. The amount of these crystals can be determined spectrophotometrically and serves as an estimate for the number of mitochondria, and hence the number of living cells in the well [70 (link)]. After 3 h of incubation, the cells were centrifuged for 5 min at 1000 g and the supernatant was removed. The obtained formazan crystals were dissolved in DMSO (100 μL) and the optical density (OD) of the samples was measured at λ = 540 and 620 nm, respectively, using ELISA Reader (iEMS Reader, Labsystems, Finland). OD₆₂₀ values were subtracted from OD₅₄₀ values. The percentage of cytostasis was calculated by using the following equation:
Values of OD_treated and OD_control correspond to the optical densities of the treated and the control cells, respectively. In each case, two independent experiments were carried out with four parallel measurements. The 50% inhibitory concentration (IC₅₀) values were determined from the dose–response curves. The curves were defined using Microcal™ Origin 2018 software: cytostasis was plotted as a function of concentration, fitted to a sigmoidal curve, and based on this curve, the half-maximal inhibitory concentration (IC₅₀) value was determined. IC₅₀ represents the concentration of a compound that is required for 50% inhibition in vitro and is expressed in micromolar units.

Gomena J., Vári B., Oláh-Szabó R., Biri-Kovács B., Bősze S., Borbély A., Soós Á., Ranđelović I., Tóvári J, & Mező G. (2023). Targeting the Gastrin-Releasing Peptide Receptor (GRP-R) in Cancer Therapy: Development of Bombesin-Based Peptide–Drug Conjugates. International Journal of Molecular Sciences, 24(4), 3400.

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Publication 2023

Bromides Cells Cytostatic Agents Electron Transport Enzyme-Linked Immunosorbent Assay Formazans Mitochondria Psychological Inhibition Reproduction Respiratory Chain Serum Sulfoxide, Dimethyl Tissues Violet, Gentian

Evaluating Cytostatic Effects of Conjugates

For determining the cytostatic effect of the conjugates, U87 cells were grown to confluency and then divided into 96-well tissue culture plates with an initial cell number of 5.0 × 10³ cells/well. After 24 h incubation at 37 °C, the cells were treated with the compounds overnight in the concentration range of 0.05–50 μM in 200 μL final volume containing 1.0 v/v% DMSO, whereas control cells were treated only with serum-free medium or with 1.0 v/v% DMSO at the same conditions. After the incubation, cells were washed twice with serum-free medium, then the cells were cultured for an additional 72 h in 10% serum-containing medium at 37 °C. Following that, MTT solution (at c = 0.37 mg/mL final concentration) was added to each well. The respiratory chain [32 (link)] and other electron transport systems [33 (link)] reduced MTT and thereby formed non-water-soluble violet formazan crystals within the cells [34 (link)]. The amount of these crystals can be determined by spectrophotometry and serves as an estimate for the number of mitochondria in addition to the number of living cells in the well [35 (link)]. After 3 h of incubation with MTT, the cells were centrifuged for 5 min at 2000 rpm and the supernatant was removed. The obtained formazan crystals were dissolved in DMSO (100 µL), and the optical density (OD) of the samples was measured at λ = 540 nm and 620 nm, respectively, using ELISA Reader (iEMS Reader, Labsystems, Finland). The OD₆₂₀ values were subtracted from the OD₅₄₀ values. The percent of cytostasis was calculated with the following equation:

Cytostatic effect (%) = 1 - \frac{{OD}_{treated}}{{OD}_{control}} \times 100

where the OD_treated and OD_control values correspond to the optical densities of the treated and the control wells, respectively. In each case, two independent experiments were carried out with four parallel measurements. Cytostasis was plotted as a function of concentration, and the half-maximal inhibitory concentration was calculated based on a sigmoid curve fitted on the data points using Microcal™ Origin 2018 software. IC₅₀ represents the concentration of a compound that is required for 50% inhibition, expressed in micromolar units.

Pethő L., Oláh-Szabó R, & Mező G. (2023). Influence of the Drug Position on Bioactivity in Angiopep-2—Daunomycin Conjugates. International Journal of Molecular Sciences, 24(4), 3106.

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Publication 2023

Cells Cytostatic Agents Electron Transport Enzyme-Linked Immunosorbent Assay Formazans Mitochondria Psychological Inhibition Reproduction Respiratory Chain Serum Sigmoid Colon Spectrophotometry Sulfoxide, Dimethyl Tissues Violet, Gentian

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Cell counting kit 8 (cck8) by Dojindo Laboratories

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What are the key considerations when using Cytostatic Agents in cancer treatment?

Cytostatic Agents are potent anti-cancer drugs that work by disrupting the cell cycle and selectively eliminating rapidly dividing tumor cells. Key considerations when using these agents include careful dosing to minimize harm to healthy tissues, monitoring for potential side effects, and integrating them into a comprehensive cancer treatment regimen along with other therapies. Proper protocl selection and optimization is crucial for maximizing the effectiveness of Cytostatic Agents.

How can researchers identify the most effective protocols for using Cytostatic Agents?

PubCompare.ai's AI-driven platform can greatly assist researchers in optimizing protocols for Cytostatic Agents. The tool allows you to efficiently screen the literatrue to identify the most reproducible and accruate protocols. Its AI analysis can highlight key differences in protocol effetiveness, enabling you to choose the best option for your specific research goals. This helps ensure you're leveraging the most effective Cytostatic Agent protocols to enhance your cancer research.

What are some common variations or types of Cytostatic Agents?

Cytostatic Agents encompass a diverse range of pharmaceutical compounds that target different stages of the cell cycle. Common types include antimetabolites that disrupt DNA synthesis, mitotic spindle poisons that interfere with cell division, and topoisomerase inhibitors that prevent DNA unwinding. Each class of Cytostatic Agent has unique mechanisms of action and is suited for different cancer types and treatment contexts. Carefully selecting the right Cytostatic Agent variation is key for optimizing anti-tumor efficacy.

More about "Cytostatic Agents"

Cytostatic agents, also known as cytotoxic agents or antineoplastic agents, are a class of pharmaceutical compounds that inhibit or prevent cell growth and division.
These agents are commonly used in the treatment of cancer, acting to disrupt the cell cycle and induce cell death in rapidly dividing tumor cells.
Cytostatic agents may target specific stages of the cell cycle, such as DNA synthesis or mitosis, to selectively eliminate cancerous cells while minimizing harm to healthy, non-dividing tissues.
These compounds play a crucial role in modern oncology, offering potent anti-tumor activity when used as part of comprehensive cancer treatment regimens.
Researchers can leverage AI-driven platforms like PubCompare.ai to optimize research protocols for cytostatic agents, effortlessly locating and comparing the most reproducible and accurate protocols and products from the literature, preprints, and patents.
Some common cytostatic agents include Cytarabine, Etoposide, and Doxorubicin.
These agents can be studied using techniques like the CellTiter 96® AQueous One Solution Cell Proliferation Assay, the Cell Counting Kit-8, and microscopy tools like the Eclipse 80i.
Researchers may also utilize staining methods like crystal violet to visualize the effects of cytostatic agents on cell growth and proliferation.
Microplate readers are often employed to quantify the results of these assays.
By optimizing research protocols and leveraging the latest tools and technologies, researchers can enhance their understanding of cytostatic agents and their potential applications in cancer therapy.
The PubCompare.ai platform can be a valuable resource in this endeavor, helping to identify the most reliable and effective protocols and products from the scientific literature.