SANDIMMUN NEORAL CAPSULES 25MG
CICLOSPORIN
What it does
Ciclosporin is a medicine that helps suppress the immune system to prevent the body from rejecting transplanted organs and to treat some autoimmune conditions.
Commonly used for: organ transplant rejection, rheumatoid arthritis, psoriasis
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Source: Pharmacy and Poisons Board · fetched 2026-01-28 21:31:52 · updated 2026-07-20 11:06:01
Drug Interactions
117Pharmacodynamic Warnings
Ciclosporin appears in TABLE 2: Drugs that cause nephrotoxicity
Ciclosporin appears in TABLE 16: Drugs that increase serum potassium
Severe (13)
Cholicacid - affects concentration
Ciclosporinaffectstheconcentrationofcholicacid.Avoid. oStudy https://www.facebook.c (Books-Courses-Medic
Ciclosporin - increases risk of immunosuppression
Filgotinib is predicted to increase the risk of immunosuppression when given with ciclosporin. Avoid.
Ciclosporin - decreases exposure
Lumacaftorispredictedtodecreasetheexposureto ciclosporin.Avoid.rTheoretical
Ciclosporin - affects exposure
Pralsetinibmightaffecttheexposuretociclosporin.Avoid. oTheoretical
Dabigatran - increases exposure
Ciclosporin is predicted to increase the exposure to thrombin inhibitors (dabigatran). Avoid.
Moderate (21)
Bictegravir - increases exposure
Ciclosporin is predicted to increase the exposure to bictegravir. Use with caution or avoid.
Calcium Channel Blockers - increases exposure
Ciclosporin moderately increases the exposure to calcium channel blockers (lercanidipine). Use with caution or avoid.
Chenodeoxycholic Acid - affects efficacy
Ciclosporin is predicted to affect the efficacy of chenodeoxycholic acid. Monitor and adjust dose.
Ciclosporin - increases concentration
Amiodarone increases the concentration of ciclosporin. Monitor concentration and adjust dose.
Ciclosporin - increases concentration
Miconazole increases the concentration of ciclosporin. Monitor and adjust dose.
Unknown (83)
Afatinib - increases exposure
Ciclosporin is predicted to increase the exposure to afatinib.
Aliskiren - increases exposure
Ciclosporin markedly increases the exposure to aliskiren. Also see TABLE 16 p. 1521
Alpelisib - increases exposure
Ciclosporinispredictedtoincreasetheexposuretoalpelisib. oTheoretical
Ambrisentan - increases exposure
Ciclosporin moderately increases the exposure to endothelin receptor antagonists (ambrisentan). Adjust ambrisentan dose, p. 199.
Anthracyclines - increases concentration
Ciclosporin increases the concentration of anthracyclines (daunorubicin, doxorubicin, epirubicin, idarubicin, mitoxantrone).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Ciclosporin is a medicine that helps suppress the immune system to prevent the body from rejecting transplanted organs and to treat some autoimmune conditions.
What it treats
- organ transplant rejection
- rheumatoid arthritis
- psoriasis
How it works
Ciclosporin works by reducing the activity of the immune system, which helps to stop it from attacking the body's own tissues or a transplanted organ.
Who it's for
Ciclosporin is for people who have had an organ transplant or those with certain autoimmune diseases.
Cautions
- • Be careful with other medicines that can harm the kidneys.
- • Watch out for medicines that can increase potassium levels in the blood.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Ciclosporin
BNF-referencedCiclosporin is an immunosuppressant medication primarily used to prevent organ rejection in transplant patients and to treat certain autoimmune disorders. It acts as a calcineurin inhibitor, effectively suppressing T cell activation and reducing the immune response. Ciclosporin is typically administered orally or intravenously and is known for its effectiveness in managing conditions such as rheumatoid arthritis, nephrotic syndrome, and severe atopic dermatitis when conventional treatments are inadequate.
Indications
- Organ transplantation (to prevent rejection)
- Severe active rheumatoid arthritis
- Nephrotic syndrome
- Severe acute ulcerative colitis refractory to corticosteroids
- Severe atopic dermatitis where conventional therapy is ineffective
Dosage
Adults: The adult dosage of ciclosporin varies based on the condition being treated. For
Mechanism of action
Ciclosporin works by binding to cyclophilin-1 within cells, forming a complex that inhibits calcineurin. This inhibition prevents the dephosphorylation and activation of the nuclear factor of activated T cells (NF-AT), thereby reducing the production of key cytokines like IL-2, which are essential for T cell activation and proliferation. Consequently, ciclosporin effectively suppresses T cell-mediated immune responses, making it beneficial in preventing transplant rejection and managing autoimmune diseases.
Pharmacodynamics
Ciclosporin exhibits potent immunosuppressive effects, particularly on T lymphocytes, which prolongs the survival of transplanted organs and bone marrow. It modulates the immune system by reducing responses that lead to allograft rejection and controlling autoimmune reactions. Clinically, ciclosporin is associated with side effects such as hypertrichosis, gingival hyperplasia, and hyperlipidemia. Renal toxicity is also a concern, necessitating careful monitoring of renal function during treatment.
Pharmacokinetics
Ciclosporin is absorbed variably from the gastrointestinal tract, and its bioavailability can be affected by food. It is extensively metabolized by the liver, primarily by cytochrome P450 enzymes, particularly CYP3A4. The drug has a long half-life and is eliminated mainly through bile and feces, with renal excretion being minimal. Monitoring blood concentrations is critical to ensure therapeutic efficacy and minimize toxicity, especially when used in conjunction with other immunosuppressants.
Contra-indications
- Malignancy (in non-transplant indications)
- Uncontrolled hypertension (in non-transplant indications)
- Uncontrolled infections (in non-transplant indications)
Adverse effects
- Hypertrichosis
- Gingival hyperplasia
- Hyperlipidemia
- Nephrotoxicity
- Increased risk of infections
- Renal impairment
- Elevated blood pressure
Interactions
- Ciclosporin + cholic acid: Severe (affects concentration)
- Ciclosporin + darifenacin: Severe (increases exposure)
- Ciclosporin + fidaxomicin: Severe (increases exposure)
- Filgotinib + ciclosporin: Severe (increases risk of immunosuppression)
- Lumacaftor + ciclosporin: Severe (decreases exposure)
- Ciclosporin + mifamurtide: Severe (decreases efficacy)
- Pralsetinib + ciclosporin: Severe (affects exposure)
- Ciclosporin + rosuvastatin: Severe (increases exposure)
- Ciclosporin + tacrolimus: Severe (increases concentration)
- Ciclosporin + thrombin inhibitors: Severe (increases exposure)
Precautions
- Monitor renal function within 2 weeks in elderly patients
- Monitor blood-ciclosporin concentrations to adjust doses
- Allow active infections to clear before starting treatment
- Use with caution in patients with hyperuricaemia and those with herpes simplex infections
Pregnancy
Ciclosporin should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is classified as category C.
Breast-feeding
Ciclosporin is excreted in breast milk. Caution is advised when administering to nursing mothers.
Storage
Store in a cool, dry place, away from light. Do not freeze.
Formulations
- Powder for solution for injection
- Oral capsules
- Oral solution
- Eye drops
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Ciclosporin
PubChem CID 5284373Molecular formula: C62H111N11O12
Mechanism of action
Cyclosporine is a calcineurin inhibitor that inhibits T cell activation. Its binding to the receptor cyclophilin-1 inside cells produces a complex known as cyclosporine-cyclophilin. This complex subsequently inhibits calcineurin, which in turn stops the dephosphorylation as well as the activation of the nuclear factor of activated T cells (NF-AT) that normally cause inflammatory reactions. NF-AT is a transcription factor that promotes the production of cytokines such as IL-2, IL-4, interferon-gamma and TNF-alpha, all of which are involved in the inflammatory process. Specifically, the inhibition of IL-2, which is necessary for T cell activation or proliferation, is believed to be responsible for cyclosporine's immunosuppressive actions. In addition to the above, the inhibition of NF-AT leads to lower levels of other factors associated with T helper cell function and thymocyte development. Cyclosporine suppresses some humoral immunity but is more effective against T cell-dependent immune mechanisms such as those underlying transplant rejection & some forms of autoimmunity. It preferentially inhibits antigen-triggered signal transduction in T lymphocytes, blunting expression of many lymphokines, including /(interleukin-2)/ IL-2, as well as expression of antiapoptotic proteins. Cyclosporine forms a complex with cyclophilin, a cytoplasmic receptor protein present in target cells. This complex binds to calcineurin, inhibiting Ca2+ stimulated dephosphorylation of the cytosolic component of NFAT. When the cytoplasmic component of NFAT is dephosphorylated, it translocates to the nucleus, where it complexes with nuclear components required for complete T-cell activation, including transactivation of IL-2 & other lymphokine genes. Calcineurin enzymatic activity is inhibited following physical interaction with the cyclosporine/cyclophilin complex. This results in the blockade of NFAT dephosphorylation; thus, the cytoplasmic component of NFAT does not enter the nucleus, gene transcription is not activated, & the T lymphocyte fails to respond to specific antigenic stimulation Cyclosporine also increases expression of transforming growth fact /beta/ (TGF-B), a potent inhibitor of IL-2-stimulated T-cell proliferation & generation of cytotoxic T lymphocytes (CTL). The exact mechanism of action is unknown but seems to be related to the inhibition of production and release of interleukin-2, which is a proliferative factor necessary for the induction of cytotoxic T lymphocytes in response to alloantigenic challenge, and which plays a major role in both cellular and humoral immune responses. Cyclosporine does not affect the nonspecific defense system of the most and does not cause significant myelosuppression. The major pharmacodynamic action of cyclosporin within T cells is calcineurin inhibition. The complex cyclophilin-cyclosporin competitively binds to the Ca(2+)- & calmodulin-dependent phosphatase calcineurin which then inhibits downstream dephosphorylation & activation of NFAT(transcription factor). The greatest calcineurin inhibition is seen 1-2 hr after admin of Neoral in parallel to the highest blood concn. Treatment of patients after organ transplantation with the immunosuppressive drug cyclosporin A (CsA) is often accompanied by impaired glucose tolerance, thus promoting the development of diabetes mellitus. ... /The authors/ show that 2-5 microM CsA diminishes glucose-induced insulin secretion of isolated mouse pancreatic islets in vitro by inhibiting glucose-stimulated oscillations of the cytoplasmic free-Ca(2+) concn [Ca(2+)](c). This effect is not due to an inhibition of calcineurin, which mediates the immunosuppressive effect of CsA, because other calcineurin inhibitors, deltamethrin & tacrolimus, did not affect the oscillations in [Ca(2+)](c) of the B-cells. The CsA-induced decr in [Ca(2+)](c) to basal values was not caused by a direct inhibition of L-type Ca(2+) channels. CsA is known to be a potent inhibitor of the mitochondr
Pharmacodynamics
Cyclosporine exerts potent immunosuppressive actions on T cells, thereby prolonging survival following organ and bone marrow transplants. This drug prevents and controls serious immune-mediated reactions including allograft rejection, graft versus host disease, and inflammatory autoimmune disease. Some notable effects of cyclosporine are hypertrichosis, gingival hyperplasia, and hyperlipidemia. There is also some debate about this drug causing nephrotoxicity.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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The same active ingredient registered across other registries we cover - including different brands.