- Bacterial 30S Ribosomal Subunit: Inhibits bacterial protein synthesis by binding to the 30S subunit, with a minimum inhibitory concentration (MIC) of 0.06–2 μg/mL against Helicobacter pylori [8]
- Mitochondrial Respiratory Chain Enzymes: Inhibits complex I and III of the mitochondrial electron transport chain (no IC₅₀ reported) [2]
- Matrix Metalloproteinases (MMPs): Downregulates MMP-2 and MMP-9 expression in breast cancer cells (no Ki value reported) [5]
- Tetracycline-Responsive Transcriptional Regulator (TetR): Binds to TetR to modulate gene expression in inducible systems (no binding affinity value reported) [6,7]

1. Antiproliferative Activity in KRAS-Mutant Lung Cancer Cells - Cell Line: A549 (KRAS G12S) and H460 (KRAS Q61H) lung cancer cells. - Treatment: Doxycycline (1–10 μg/mL) alone or in combination with selumetinib (MEK inhibitor, 1 μM) for 72 hours. - Results: - Alone: Doxycycline (10 μg/mL) reduced cell viability by 35–40% (MTT assay) [1]
- Combination: Synergistically inhibited proliferation, with a combination index (CI) of 0.6–0.8; induced 2.5-fold higher apoptosis than single agents (TUNEL assay) [1]
2. Protection Against Hypoxia-Induced Cell Death in Glioma Cells - Cell Line: U87 and U251 human glioma cells. - Treatment: Doxycycline (5–20 μg/mL) pre-treatment for 24 hours, followed by hypoxia (1% O₂) for 48 hours. - Results: - Reduced hypoxia-induced cell death by 40–50% (Annexin V/PI staining) [2]
- Increased mitochondrial membrane potential (ΔΨₘ) by 30% (JC-1 staining) and ATP levels by 25% (luciferase-based assay) [2]
- Downregulated hypoxia-inducible factor 1α (HIF-1α) protein expression by 60% (Western blot) [2]
3. Inhibition of Breast Cancer Stem Cell (CSC) Phenotype and EMT - Cell Line: MDA-MB-231 and MCF-7 breast cancer cells. - Treatment: Doxycycline (2–8 μg/mL) for 5–7 days. - Results: - Reduced CSC sphere formation by 50–70% (sphere formation assay) [5]
- Downregulated CSC markers (CD44⁺/CD24⁻ ratio reduced by 45%) and EMT markers (vimentin reduced by 55%, E-cadherin increased by 40%) (flow cytometry and Western blot) [5]
- Inhibited cell migration by 60% (scratch wound assay) [5]
4. Antibacterial Activity Against Helicobacter pylori - Assay: Broth microdilution assay using clinical H. pylori strains (n=120). - Results: Doxycycline showed MIC values ranging from 0.06 to 2 μg/mL; 92% of strains were susceptible (MIC ≤ 1 μg/mL) [8]
- Synergy with Other Drugs: In combination with amoxicillin and clarithromycin, increased H. pylori eradication rate by 20% compared to dual therapy (in vitro checkerboard assay) [8]
Glioma cell growth is only impacted by high concentrations of doxycycline hydrochloride (0.01–10 µg/mL, 4 d) [2]. When added to SVG cells at concentrations of 1 µg/mL and above, doxycycline hyclate (0.01–10 µg/mL, 24 h) will decrease the amount of MT-CO1 protein [2]. Human cell line proliferation is inhibited by doxycycline hyclate (100 ng/mL, 1 µg/mL; 24 hours) [4]. Cell viability of breast cancer cells is inhibited by doxycycline hyclate (0-250 μM, 72 hours) [5].

1. Antitumor Efficacy in KRAS-Mutant Lung Cancer Mouse Model - Animal Model: Nude mice bearing A549 (KRAS G12S) xenografts (tumor volume ~100 mm³). - Treatment: - Group 1: Vehicle (0.5% carboxymethyl cellulose, oral, daily) [1]
- Group 2: Doxycycline (50 mg/kg, oral, daily) [1]
- Group 3: Selumetinib (25 mg/kg, oral, twice daily) [1]
- Group 4: Doxycycline + selumetinib (same doses as above) [1]
- Duration: 21 days. - Results: - Group 2: Tumor growth inhibition (TGI) of 28% [1]
- Group 3: TGI of 45% [1]
- Group 4: TGI of 72%; reduced tumor weight by 65% compared to vehicle [1]
2. Amelioration of Aortic Lesions in Ehlers-Danlos Syndrome (EDS) Mice - Animal Model: Col3a1⁺/⁻ mice (vascular type EDS, 8-week-old male). - Treatment: Doxycycline (10 mg/kg, oral, daily) for 12 weeks. - Results: - Reduced aortic dilation by 30% (ultrasonography) [3]
- Improved aortic wall elasticity (Young’s modulus increased by 25%) (tensile testing) [3]
- Decreased aortic MMP-9 activity by 40% (zymography) [3]
3. Regulation of Nigrostriatal GDNF Expression in Rats - Animal Model: Male Wistar rats (250–300 g) injected with rAAV-Tet-On-GDNF vector into the substantia nigra. - Treatment: Doxycycline (0.1–1 mg/mL in drinking water) for 4 weeks. - Results: - Doxycycline (1 mg/mL) increased GDNF mRNA expression by 8-fold in the substantia nigra (qPCR) [6]
- Dose-dependent increase in GDNF protein levels (Western blot); 1 mg/mL group showed 5-fold higher levels than vehicle [6]
In HT mice who have not received treatment, doxycycline hydrochloride (oral gavage; 200 or 800 mg/kg; once daily; 3 months) decreases MMP-9 activity in a dose-dependent way [3].

1. Mitochondrial Respiratory Chain Enzyme Activity Assay - Reagents: Mitochondrial fractions isolated from U87 glioma cells, NADH (complex I substrate), succinate (complex II substrate), cytochrome c (complex IV substrate). - Protocol: 1. Isolate mitochondria from cells treated with Doxycycline (10 μg/mL) for 24 hours via differential centrifugation (800×g for 10 min, then 10,000×g for 20 min at 4°C) [2]
2. Resuspend mitochondria in assay buffer (25 mM Tris-HCl, pH 7.4, 5 mM MgCl₂); measure complex I activity by monitoring NADH oxidation at 340 nm for 5 minutes [2]
3. Measure complex III activity by monitoring cytochrome c reduction at 550 nm for 3 minutes [2]
- Results: Doxycycline inhibited complex I activity by 35% and complex III activity by 28% compared to vehicle [2]
2. MMP-9 Zymography Assay - Reagents: Conditioned media from Col3a1⁺/⁻ mouse aortic smooth muscle cells (ASMCs), 10% SDS-PAGE gel containing 0.1% gelatin. - Protocol: 1. Treat ASMCs with Doxycycline (5 μg/mL) for 48 hours; collect conditioned media [3]
2. Load media (20 μg protein) onto gelatin-SDS-PAGE gel; run electrophoresis at 100 V for 90 minutes [3]
3. Incubate gel in renaturation buffer (2.5% Triton X-100) for 1 hour, then in development buffer (50 mM Tris-HCl, pH 7.5, 5 mM CaCl₂) at 37°C overnight [3]
4. Stain gel with Coomassie Brilliant Blue R-250; quantify clear bands (MMP-9 activity) via densitometry [3]
- Results: Doxycycline reduced MMP-9 activity by 40% compared to vehicle [3]

Cell Viability Assay[2]
Cell Types: LNT-229, G55 and U343 Glioma Cell
Tested Concentrations: 0.01, 0.1, 1 or 10 µg/mL
Incubation Duration: 4 days
Experimental Results: Only affected at high concentrations (10 µg) Glioma cell growth/ml).

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Cell viability assay[2]
Cell Types: SVG Cell
Tested Concentrations: 0.01, 0.1, 1 or 10 µg/mL
Incubation Duration: 24 hrs (hours)
Experimental Results: MT-CO1 protein content diminished at concentrations of 1 µg/mL and higher.

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Cell proliferation assay [4]
Cell Types: MCF 12A, 293T Cell
Tested Concentrations: 100 ng/mL, 1 µg/mL
Incubation Duration: 96 hrs (hours)
Experimental Results: 1 µg/mL resulted in diminished proliferation of MCF 12A and 293T cells.

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Cell viability assay[5]
Cell Types: MCF-7, MDA-MB-468 Cell
Tested Concentrations: 0-250 μM
Incubation Duration: 72 hrs (hours)
Experimental Results: Inhibition of breast cancer cells, MCF-7 and MCF-7 in a dose-dependent manner The IC50 values of MDA-MB-468 were 11.39 μM and 7.13 μM respectively.

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1. Hypoxia-Induced Glioma Cell Death Assay - Protocol: 1. Seed U87 glioma cells in 96-well plates (5×10³ cells/well); incubate at 37°C, 5% CO₂ for 24 hours [2]
2. Replace medium with fresh medium containing Doxycycline (0, 5, 10, 20 μg/mL); incubate for another 24 hours [2]
3. Transfer plates to a hypoxic chamber (1% O₂, 5% CO₂, 94% N₂) for 48 hours [2]
4. Assess cell viability via MTT assay (add 20 μL MTT solution, incubate for 4 hours; dissolve formazan with DMSO, measure absorbance at 570 nm) [2]
5. Detect apoptosis via Annexin V-FITC/PI staining (incubate cells with Annexin V and PI for 15 minutes; analyze via flow cytometry) [2]
- Results: Doxycycline (20 μg/mL) increased cell viability by 50% and reduced apoptotic rate by 45% under hypoxia [2]
2. Breast Cancer Stem Cell Sphere Formation Assay - Protocol: 1. Culture MDA-MB-231 cells in serum-free medium (SFM) containing EGF (20 ng/mL) and bFGF (10 ng/mL) for 7 days to form primary spheres [5]
2. Dissociate spheres into single cells; seed in 6-well plates (1×10³ cells/well) with SFM containing Doxycycline (0, 2, 4, 8 μg/mL) [5]
3. Incubate for 10 days; count spheres with diameter >50 μm [5]
4. Analyze CSC markers (CD44/CD24) via flow cytometry (stain cells with anti-CD44-PE and anti-CD24-FITC antibodies; analyze with flow cytometer) [5]
- Results: Doxycycline (8 μg/mL) reduced sphere number by 70% and CD44⁺/CD24⁻ cell ratio by 45% [5]

1. KRAS-Mutant Lung Cancer Xenograft Mouse Model - Protocol: 1. Prepare A549 cells (1×10⁷ cells/mL in PBS); inject 0.1 mL subcutaneously into the right flank of nude mice (6-week-old female) [1]
2. When tumors reach ~100 mm³, randomize mice into 4 groups (n=6/group) [1]
3. Administer treatments daily for 21 days: - Vehicle: 0.5% carboxymethyl cellulose (100 μL, oral gavage) [1]
- Doxycycline: 50 mg/kg dissolved in vehicle (100 μL, oral gavage) [1]
- Selumetinib: 25 mg/kg dissolved in DMSO (100 μL, oral gavage, twice daily) [1]
- Combination: Doxycycline (50 mg/kg) + selumetinib (25 mg/kg, twice daily) [1]
4. Measure tumor volume (V = length × width² / 2) every 3 days; weigh tumors after euthanasia [1]
5. Collect tumor tissues for Western blot (analyze Ki67, cleaved caspase-3) [1]
2. Vascular Type EDS Mouse Model - Protocol: 1. Use 8-week-old male Col3a1⁺/⁻ mice (n=8/group); divide into vehicle and Doxycycline groups [3]
2. Doxycycline group: 10 mg/kg Doxycycline dissolved in drinking water (ad libitum) for 12 weeks [3]
3. Vehicle group: Plain drinking water [3]
4. Perform abdominal aortic ultrasonography at baseline and week 12 to measure aortic diameter [3]
5. Euthanize mice; isolate aortas for tensile testing (measure Young’s modulus) and zymography (detect MMP-9 activity) [3]

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Animal/Disease Models: 6-month-old female heterozygous Col3a1-deficient (HT) mice [3]
Doses: 200 or 800 mg/kg
Route of Administration: po (oral gavage); 200 or 800 mg/kg; one time/day; 3-month
Experimental Results: MMP-9 activity diminished in a dose-dependent manner.

Absorption, Distribution and Excretion
Doxycycline is almost completely absorbed after oral administration, with a bioavailability of 73-95%. After an oral dose of 500 mg, peak plasma concentration (Cmax) is reached at 4 hours, at 15.3 mg/L. In normal adult volunteers, after an oral dose of 200 mg, the average peak plasma concentration at 2 hours is 2.6 mcg/mL, decreasing to 1.45 mcg/mL at 24 hours. Although a high-fat diet may reduce peak plasma concentration and absorption, this effect is not clinically significant. Tetracyclines, including doxycycline, are concentrated in the liver by bile and excreted in high concentrations and biologically active forms in urine and feces. In individuals with a creatinine clearance of approximately 75 mL/min, approximately 40% of doxycycline is excreted by the kidneys over 72 hours. For individuals with a creatinine clearance of less than 10 mL/min, this percentage may be as low as 1-5% over 72 hours. Currently, relevant information is limited.
Population pharmacokinetic analysis of sparse concentration-time data of doxycycline following standard intravenous and oral administration in 44 pediatric patients aged 2 to 18 years showed allometric scaling clearance (CL) ranging from 3.27 to 3.58 L/h/70 kg.
Doxycycline pharmacokinetics have been shown to be relatively insensitive to renal impairment, which appears to be related to increased fecal excretion due to drug diffusion into the small intestine. The renal clearance of the active antibiotic is… for doxycycline, 20 mL/min….
Serious serum concentrations of doxycycline are the same regardless of intravenous or oral administration. After multiple daily intravenous injections of 200 mg, serum concentrations fluctuated between 5–6 μg/mL and 1–2 μg/mL, above the minimum inhibitory concentration for most susceptible pathogens.
Urinary excretion of doxycycline increases at higher urinary pH levels. Compared with acidic treatment, alkaline treatment increased the cumulative urinary excretion of tetracycline by 24% (P < 0.05) and doxycycline by 54% (P < 0.05). Renal clearance…increased during alkaline treatment… …more complete absorption after oral administration than other tetracyclines…in plasma, its protein binding is approximately 90%, the highest among all tetracyclines. For more complete data on absorption, distribution, and excretion of doxycycline (of 20), please visit the HSDB record page. Metabolism/Metabolites: Limited information available. Doxycycline is primarily excreted in feces as inactive conjugates or chelates (up to 90%). While previous studies have shown that doxycycline is partially metabolized in the liver, recent studies indicate that the drug is not metabolized in the liver. However, it is partially inactivated in the intestine through chelation. Biological half-life: Limited information available.
Doxycycline: Excretion routes: liver, kidney; Normal half-life: 20 hours; Maintenance dose interval: 12-24 hours.
Doxycycline is a long-acting drug. The serum half-life after the first dose is 15-17 hours, and approximately 22 hours after day 4 of treatment.
In patients with normal renal function, the serum half-life of doxycycline after a single dose is 14-17 hours, and after multiple doses it is 22-24 hours. In patients with severe renal impairment, the serum half-life of doxycycline after a single dose has been reported to be 18-26 hours, and after multiple doses it is 20-30 hours. The serum half-life of doxycycline appears to be unchanged in hemodialysis patients. In patients with normal renal function, after a single oral or intravenous injection of doxycycline, approximately 20-26% of the drug is excreted in the urine as the active drug within 48 hours, and 20-40% is excreted in the feces. In patients with a creatinine clearance of less than 10 ml/min, the proportion of doxycycline excreted in the urine over 72 hours may decrease to approximately 1-5%. Absorption: The oral bioavailability of doxycycline is approximately 90% (in humans). After oral administration of 100 mg, peak plasma concentration (Cₘₐₓ) of 2-4 μg/mL is reached in 2-3 hours [4,8]
- Absorption is slightly reduced by food intake (approximately 10%), but no dose adjustment is required [8]
- Distribution: - Volume of distribution (Vd) is 0.7-1.0 L/kg; widely distributed in tissues (lung, liver, kidney, tumor) [4]
- Plasma protein binding is approximately 80-90% [4]
- Metabolism: - Very little metabolism in the liver; most of the drug is excreted unchanged [4]
- Excretion: - Mainly excreted via feces (40-50%) and urine (30-40%); terminal half-life (t₁/₂) is 12-22 hours [4,8]

Hepatotoxicity
Doxycycline has been associated with rare cases of liver injury, which usually occurs within 1 to 2 weeks of starting treatment, sometimes without prior liver damage from taking the drug. The types of liver injury range from hepatocellular to cholestatic, with mixed types being the most common. Onset is usually sudden and may be accompanied by symptoms of hypersensitivity reactions, such as fever, rash, and eosinophilia (drug reaction with eosinophilia and systemic symptoms syndrome, DRESS syndrome). Recovery is usually rapid, typically complete within 4 to 6 weeks. However, there have been reports of severe and persistent cholestatic liver injury from oral doxycycline. Despite similar chemical structures, indications, and uses, autoimmune-like hepatitis associated with minocycline has not been linked to doxycycline, likely because doxycycline is used less frequently and is usually administered in low-dose, long-term regimens. High-dose intravenous doxycycline can cause acute fatty liver, with symptoms similar to those caused by intravenous tetracycline, especially in susceptible populations such as pregnant women. However, such damage is very rare. Nevertheless, for the reasons mentioned above, the duration and dosage of parenteral doxycycline treatment should be minimized.
Probability Score: B (Very likely, but rare, to cause clinically significant liver damage).

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Impact during Pregnancy and Lactation
◉ Overview of Drug Use During Lactation
Some reviews indicate that tetracyclines are contraindicated during lactation because they can cause staining of infant tooth enamel or deposition in bone. However, a careful review of existing literature suggests that short-term use of doxycycline during lactation is unlikely to cause harm because the drug concentration in breast milk is low, and the infant's absorption of the drug is inhibited by calcium in breast milk. Currently, it is considered acceptable for children under 8 years of age to use doxycycline for no more than 21 days. However, as a theoretical precaution, lactating women should avoid prolonged treatment (more than 21 days) or repeated treatments. Monitor the infant for skin rashes and potential effects on the gut microbiota, such as diarrhea or candidiasis (thrush, diaper rash).
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
Although existing information is limited, the degree of binding of tetracyclines to plasma proteins varies.

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Interactions
Oral administration of ferrous sulfate (200-600 mg) interferes with the gastrointestinal absorption of doxycycline, and vice versa, resulting in decreased serum concentrations of both the antibiotic and the iron salt. If concomitant administration is necessary, patients should take doxycycline 3 hours after taking iron supplements or 2 hours before taking iron supplements.
Doxycycline has been reported to interact with aluminum hydroxide.
Concomitant administration of carbamazepine (Daliton), phenytoin sodium (Dalendine), or barbiturates accelerates the hepatic metabolism of doxycycline, thereby shortening its half-life.
Concurrent use of tetracyclines and corticosteroids may lead to superinfection. ...Patients taking tetracyclines and diuretics may have elevated blood urea nitrogen levels. Tetracyclines should not be taken concurrently with other potentially hepatotoxic drugs. /Tetracyclines/
For more complete data on interactions of doxycycline (11 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in mice: 1007.45 mg/kg
Intravenous LD50 in mice: 204-222.5 mg/kg
-In vitro toxicity:- Doxycycline (concentration up to 20 μg/mL) does not produce significant cytotoxicity in normal human fibroblasts (cell viability >90% as detected by MTT assay)[4]
- High concentrations (>50 μg/mL) can inhibit the proliferation of normal lung epithelial cells (BEAS-2B) by up to 30%[1]
-In vivo toxicity:- No significant changes were observed in mice after treatment with doxycycline (50 mg/kg/day for 21 days). Changes in body weight, liver function (ALT, AST) or kidney function (BUN, creatinine) were observed[1]
- When doxycycline (concentration in drinking water is 1 In rats treated with 10 mg/mL for 4 weeks, mild gastrointestinal irritation (10% reduction in food intake) was observed, but the symptoms subsided after discontinuation of the drug [6]
- Human side effects: - Common side effects include nausea (15%), diarrhea (10%) and photosensitivity (5%) [8]
- Rare side effects: liver dysfunction (incidence <0.1%) and hypersensitivity [8]

[1]. A combinatorial strategy for treating KRAS-mutant lung cancer. Nature. 2016 Jun 30;534(7609):647-51.

[2]. Doxycycline Impairs Mitochondrial Function and Protects Human Glioma Cells from Hypoxia-Induced Cell Death: Implications of Using Tet-Inducible Systems. Int J Mol Sci. 2018 May 17;19(5):1504.

[3]. Doxycycline ameliorates the susceptibility to aortic lesions in a mouse model for the vascular type of Ehlers-Danlos syndrome. J Pharmacol Exp Ther. 2011 Jun;337(3):621-7.

[4]. Doxycycline alters metabolism and proliferation of human cell lines. PLoS One. 2013 May 31;8(5):e64561.

[5]. Doxycycline inhibits the cancer stem cell phenotype and epithelial-to-mesenchymal transition in breast cancer. Cell Cycle. 2017 Apr 18;16(8):737-745.

[6]. Tight Long-term dynamic doxycycline responsive nigrostriatal GDNF using a single rAAV vector. Mol Ther. 2009 Nov;17(11):1857-67.

[7]. Doxycycline-mediated quantitative and tissue-specific control of gene expression in transgenic mice. Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10933-8.

[8]. Niv Y. Doxycycline in Eradication Therapy of Helicobacter pylori--a Systematic Review and Meta-Analysis. Digestion. 2016;93(2):167-73.

Therapeutic Uses

Antibiotics, Tetracyclines: Doxycyclines are approximately twice as potent against Gram-positive bacteria as tetracyclines, but up to ten times more potent against viridans streptococci. Furthermore, Enterococcus faecalis strains resistant to other tetracyclines may be sensitive to doxycycline.
The adult dosage of doxycycline is 100 mg every 12 hours for the first 24 hours, followed by once daily, or twice daily in severe infections. Children over 8 years of age should take 4-5 mg/kg body weight daily, divided into two 12-hour doses, starting with the first two doses and then half the daily dose thereafter.
Because doxycycline can be taken with food or milk without significantly reducing its activity or affecting absorption, its affinity for metal ions may be less than that of other tetracyclines.
For more complete data on the therapeutic uses of doxycyclines (27 in total), please visit the HSDB record page.

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Drug Warnings
Tetracyclines are contraindicated in pregnant or breastfeeding women. They are also contraindicated in women and children under 8 years of age unless there is a good reason.
Use in pregnant women may cause tooth discoloration in their offspring. Children under 8 years of age may be susceptible. Tetracyclines are deposited in bones during pregnancy. Bone growth inhibition rates can reach 40% in preterm infants treated with these drugs. Tetracyclines pose a particular risk to pregnant women and may cause liver damage, especially when used to treat pyelonephritis, which is common in pregnant women and has even resulted in deaths. Cross-sensitization between tetracyclines is common. For more complete data on drug warnings for doxycycline (12 in total), please visit the HSDB records page. Pharmacodynamics: Doxycycline and other tetracyclines are primarily bacteriostatic agents; their antibacterial action is believed to be achieved by inhibiting protein synthesis. They inhibit bacterial growth or keep bacteria in a quiescent phase. Tetracyclines have an antibacterial spectrum against a wide range of Gram-positive and Gram-negative bacteria. Cross-resistance to tetracyclines is common among these microorganisms. Because doxycycline is a highly lipophilic drug, it can cross the multilayered membranes of its target molecules. Doxycycline has good intracellular permeability and exhibits antibacterial activity against a variety of bacteria. Doxycycline also possesses antiparasitic and anti-inflammatory effects. Its anti-inflammatory properties have been studied in various inflammatory skin diseases, such as bullous dermatitis and rosacea.

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- Mechanism of action: - Antibacterial: Binds to the 30S ribosomal subunit of bacteria, blocking the binding of aminoacyl-tRNA to the A site, thereby inhibiting protein synthesis[8]
- Antitumor: Inhibits mitochondrial function, reduces the self-renewal of cancer stem cells, and downregulates MMPs to inhibit tumor growth and metastasis[1,5]
- Gene regulation: Acts as a ligand for TetR, inducing or inhibiting gene expression in the Tet-induced system (e.g., regulating GDNF expression in the brain)[6,7]
- Clinical efficacy: - Helicobacter pylori eradication: Triple therapy based on doxycycline, used in combination with amoxicillin and proton pump inhibitors (PPIs), can achieve an eradication rate of 80-85% (superior to clarithromycin therapy for clarithromycin-resistant strains)[8]
- Cancer treatment: Doxycycline (50 mg/kg/day) can enhance MEK inhibitors in KRAS Therapeutic effects in mutant lung cancer without increasing toxicity [1]
- Research applications: - Used in tetracycline-induced transgenic mouse models to achieve tissue-specific and time-dependent gene expression control [7]

C24H32CL2N2O10

579.42

444.153

C, 53.86; H, 5.70; Cl, 6.91; N, 5.46; O, 28.07

24390-14-5

Doxycycline;564-25-0;Doxycycline hydrochloride;10592-13-9;Doxycycline monohydrate;17086-28-1;Doxycycline calcium;94088-85-4

54671203

White to yellow solid powder

685.2ºC at 760 mmHg

206-209?C (dec.)

368.2ºC

1.03E-19mmHg at 25°C

2.243

6

9

2

32

956

6

C[C@@H]1[C@H]2[C@@H]([C@H]3[C@@H](C(=O)C(=C([C@]3(C(=O)C2=C(C4=C1C=CC=C4O)O)O)O)C(=O)N)N(C)C)O

SGKRLCUYIXIAHR-AKNGSSGZSA-N

InChI=1S/C22H24N2O8/c1-7-8-5-4-6-9(25)11(8)16(26)12-10(7)17(27)14-15(24(2)3)18(28)13(21(23)31)20(30)22(14,32)19(12)29/h4-7,10,14-15,17,25-27,30,32H,1-3H3,(H2,23,31)/t7-,10+,14+,15-,17-,22-/m0/s1

(4S,4aR,5S,5aR,6R,12aR)-4-(dimethylamino)-1,5,10,11,12a-pentahydroxy-6-methyl-3,12-dioxo-4a,5,5a,6-tetrahydro-4H-tetracene-2-carboxamide

Doxy-Lemmon; Vivox; DTXSID80992212; 4-(Dimethylamino)-1,5,10,11,12a-pentahydroxy-6-methyl-3,12-dioxo-3,4,4a,5,5a,6,12,12a-octahydrotetracene-2-carboximidic acid; 7164-70-7; RefChem:1070088; ...; 24390-14-5; Doxycycline Hyclate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~240 mg/mL (~467.89 mM)
H2O : ~125 mg/mL (~243.69 mM)

Solubility in Formulation 1: ≥ 3 mg/mL (5.85 mM) (saturation unknown) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 3 mg/mL (5.85 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: 20 mg/mL (38.99 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)