Itraconazole Capsule 100 Mg

Itraconazole capsule 100 mg are a broad-spectrum antifungal drug belonging to the triazole derivative class. Its core mechanism of action is to inhibit the synthesis of ergosterol, a key component of fungal cell membranes, disrupting the integrity and permeability of the cell membrane, leading to leakage of fungal cell contents and death. As a reliable supplier of research chemical raw materials, Bloomtechz supplies research-grade Itraconazole capsule 100 mg with stable batch quality and complete test documentation, supporting in-vitro antifungal mechanism research and related laboratory studies.

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Certificate of Analysis
Compound name	Itraconazole
Grade	Pharmaceutical grade
CAS No.	84625-61-6
Quantity	18g
Packaging standard	PE bag+Al foil bag
Manufacturer	Shaanxi BLOOM TECH Co., Ltd
Lot No.	202601090055
MFG	Jan 9th 2026
EXP	Jan 8th 2029
Structure
Item	Enterprise standard	Analysis result
Appearance	White or almost white powder	Conformed
Water content	≤5.0%	0.87%
Loss on drying	≤1.0%	0.56%
Heavy Metals	Pb≤0.5ppm	N.D.
	As≤0.5ppm	N.D.
	Hg≤0.5ppm	N.D.
	Cd≤0.5ppm	N.D.
Purity (HPLC)	≥99.0%	99.53%
Single impurity	<0.8%	0.74%
Total microbial count	≤750cfu/g	527
E. Coli	≤2MPN/g	N.D.
Salmonella	N.D.	N.D.
Ethanol (by GC)	≤5000ppm	543ppm
Storage	Store in a sealed, dark, and dry place below 2-8°C

As a representative of triazole broad-spectrum antifungal drugs, itraconazole capsule 100 mg achieve efficient antifungal activity through multi-target synergistic action. This drug forms a multi-layered antibacterial barrier by inhibiting the synthesis of key components of fungal cell membranes, interfering with energy metabolism, disrupting cell wall integrity, and regulating host immune responses.

Core mechanism of action: inhibition of ergosterol synthesis

 

1.1 Precise blockade of sterol synthesis pathway
The stability of fugal cell membranes depends on the specific presence of ergosterol, and its synthesis process involves the conversion of lanosterol to ergosterol. Itraconazole blocks the conversion of lanosterol to 14 α - demethylated lanosterol by binding to cytochrome P450 dependent 14 α - demethylase (CYP51) with high affinity. This step is the rate limiting step in the biosynthesis of ergosterol. Drug action leads to abnormal accumulation of lanosterol in the cell membrane, while the accumulation of ergosterol precursor 24 methylene dihydrolanosterol further interferes with membrane fluidity.

 

1.2 Dual destruction of cell membrane structure and function
Lack of ergosterol leads to significant changes in cell membrane permeability
Decreased membrane fluidity: The interaction between ergosterol and phospholipid molecules weakens, leading to abnormal distribution of membrane proteins
Material transport disorders: ATP dependent ion pump function impaired, increased intracellular potassium ion efflux
Membrane integrity collapse: Electron microscopy observation shows significant vesiculation of Candida albicans cell membrane after 24 hours of treatment
This structural damage directly leads to leakage of fungal cell contents. Clinical studies have shown that itraconazol has a minimum inhibitory concentration (MIC) range of 0.01-0.5 μ g/mL for Candida and 0.25-2 μ g/mL for Aspergillus, demonstrating its potent antibacterial activity.

Synergistic mechanism: multi-target interference in fugal metabolism

 

2.1 Inhibition of cell wall synthesis
Itraconazole inhibits the cross-linking of β - glucan, the main component of the cell wall, by downregulating the expression of the β -1,3-glucan synthase gene (FKS1). Scanning electron microscopy observation showed that after 72 hours of treatment, obvious pores appeared in the cell wall of Aspergillus fumigatus, and the content of pectin decreased by 40% -60%. This effect forms a synergistic effect with echinocandins, providing a theoretical basis for combination therapy.
2.2 Energy metabolism interference
The drug inhibits mitochondrial respiratory chain complex III and blocks ATP synthesis:
Decreased oxygen consumption rate: Candida albicans reduced oxygen consumption by 65%
ATP levels decrease: intracellular ATP concentration drops from the normal value of 3.2 mmol/g to 0.8 mmol/g

 

Metabolic intermediate volume accumulation: Succinic acid, an intermediate product in the citric acid cycle, accumulates up to three times the normal level
This metabolic inhibition leads to fungal growth arrest in the G1 phase and a decrease of over 80% in cell division index.

2.3 Blockage of biofilm formation
Itraconazol can inhibit the expression of key genes involved in biofilm formation in Candida albicans, such as ALS3 and HWP1
Reduction in biofilm thickness: Laser confocal microscopy measurement shows a decrease in thickness from 120 μ m to 35 μ m
Reduction of extracellular matrix: polysaccharide content decreased by 70%
Enhanced drug penetration: Drug concentration within the biofilm increases by 4-6 times
This characteristic makes it of special therapeutic value for refractory catheter-related infections.

Immune regulatory mechanism: host drug synergistic effect

 

3.1 Pattern recognition receptor activation
Itraconazol can upregulate the expression of Toll like receptor (TLR) 2/4 and enhance the recognition ability of macrophages towards β - glucan. The experiment showed that after drug treatment, the phagocytic index of macrophages increased from 1.2 to 3.8, and the production of reactive oxygen species (ROS) increased by 2.5 times.
3.2 Cytokine regulation
By inhibiting IL-10 secretion while promoting IL-12 and TNF - α release, drugs can reverse Th2 type immune shift. In the cryptococcal meningitis model, the level of IFN - γ in cerebrospinal fluid of the itraconazol treatment group increased fivefold compared to the control group, and the fugal clearance rate increased by 60%.

 

3.3 Enhancement of neutrophil function
Drugs can enhance the ability of neutrophils to form extracellular traps (NETs):
Increased DNA release: Flow cytometry analysis showed that the proportion of NETs positive cells increased from 15% to 42%
Enhanced bactericidal activity of histones: Histone H2A increases the bactericidal efficiency of Aspergillus by three times
This immune enhancing effect is particularly important in immunocompromised patients, as it can reduce the incidence of disseminated infections.

As a broad-spectrum triazole antifungal drug, itraconazole capsule 100 mg has been widely used in clinical practice, but its oral formulations (such as capsules) still have problems such as large fluctuations in bioavailability, uneven distribution of target organs, and decreased efficacy of drug-resistant strains. In the future, breakthroughs are needed in formulation innovation, molecular modification, and immune synergistic therapy to enhance efficacy, reduce toxicity, and delay the development of drug resistance. Based on the characteristics of the dosage form, a systematic exposition will be provided on its future research directions.

Traditional itraconazol capsules have low drug solubility and significant first pass effects, resulting in a bioavailability of only about 55% (on an empty stomach) to 65% (after a high-fat diet), with significant individual differences. Nanotechnology can significantly improve the oral absorption efficiency of drugs by regulating their particle size and surface properties.

Mutations in the target enzymes CYP51 (such as Y132F, G448S) of drug-resistant fungi (such as azole resistant Candida) lead to a decrease in the binding affinity of itraconazol. Enhancing drug activity or improving pharmacokinetic properties through chemical modification is the key to overcoming drug resistance.

With the continuous emergence of multidrug-resistant bacteria, traditional antimicrobial agents gradually suffer from reduced efficacy and unstable bactericidal performance due to fixed molecular structures and single targeting mechanisms. To solve the drug resistance dilemma,Bloomtechz focuses on molecular structural optimization research for antibacterial compounds, carrying out precise modification and directional optimization on key molecular scaffolds. By adjusting molecular polarity, binding affinity, and spatial conformation, our optimized structures effectively enhance the binding ability with bacterial target sites, weaken bacterial drug resistance mutation tolerance, and significantly improve antibacterial activity against drug-resistant strains.

This structural optimization strategy effectively breaks through the resistance mechanism of common drug-resistant bacteria, provides high-efficiency compound solutions for antimicrobial resistance research, and supports the development of new-generation anti-resistance antibacterial materials and pharmaceutical precursors.

Combination immunotherapy has become a cutting-edge research direction in modern biomedical and anti-infection studies, aiming to trigger and amplify the body's innate and adaptive immune responses rather than relying solely on single drug inhibition.

Bloomtechz focuses on the research and supply of high-purity immunomodulatory compounds for combination immunotherapy exploration. By synergistically regulating multiple immune pathways, our research-grade products effectively activate host defense mechanisms, enhance immune cell proliferation, improve pathogen clearance capability, and reverse immune suppression caused by infection or tumor microenvironments. Different from single-agent treatment, combination immunotherapy achieves coordinated immune activation, significantly improves therapeutic response efficiency, reduces drug resistance risks, and provides reliable experimental support for the development of new immune combination regimens, anti-tumor and anti-infection immune research worldwide.

The future development of itraconazole capsules requires the integration of nanotechnology, chemical modification, and immunotherapy to construct a "drug carrier host" integrated treatment system. Nanoformulations can improve oral absorption efficiency, structural optimization can overcome drug resistance, and immunotherapy can activate host defense mechanisms. In the future, interdisciplinary collaboration (such as materials science, synthetic chemistry, immunology) is needed to accelerate the translation of laboratory results into clinical practice, ultimately achieving precision, personalization, and long-term effectiveness of antifungal therapy.For example, the development of SLNs encapsulated fluconazole prodrug capsules combined with PD-1 inhibitors for the treatment of drug-resistant invasive fugal diseases is expected to become the standard protocol for the next generation of antifungal treatments.

Itraconazole capsule 100 mg occupy an important position in the field of antifungal therapy through a multi-level and multi-target antibacterial mechanism. Its mechanism of action involves multiple aspects such as cell membrane disruption, metabolic interference, and immune regulation, reflecting both the molecular characteristics of the drug itself and closely related to the host's immune status. With the deepening understanding of drug resistance mechanisms and drug interactions, as well as the continuous development of new formulation technologies, the clinical application of itraconazole will become more precise and efficient, providing a stronger weapon for the treatment of fugal infections.

Van Cutsem, J., Van Gerven, F., & Odds, F. C. (1996). Itraconazole, a new triazole antifungal agent: A review of its spectrum of activity, pharmacology and clinical use. Journal of Antimicrobial Chemotherapy, 37(1), 1–22.

Sheehan, D. J., Hitchcock, C. A., & Sibley, C. M. (1999). Current and emerging azole antifungal agents. Clinical Microbiology Reviews, 12(1), 40–79.

Gupta, A. K., & Lyons, D. C. (2003). Itraconazole capsule: Pharmacokinetics, efficacy and safety profile in superficial and systemic fungal infections. American Journal of Clinical Dermatology, 4(6), 379–394.

Vanden Bossche, H. (1985). Biochemical targets of antifungal azoles: Inhibition of ergosterol biosynthesis. Antimicrobial Agents and Chemotherapy, 27(1), 1–8.

Pappas, P. G., Kauffman, C. A., & Andes, D. (2016). Clinical practice guidelines for the management of candidiasis: 2016 update by the infectious diseases society of america. Clinical Infectious Diseases, 62(4), e1–e50.

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