Pimecrolimus 1% cream
Requires a prescription from a doctor or prescriber
Pimecrolimus is an immunomodulating agent that was first marketed by Novartis under the trade name Elidel.
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Suspected adverse reactions reported for Pimecrolimus
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2 branded products available
MHRA licensed products
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Elidel 1% cream
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Tacrolimus and pimecrolimus for atopic eczema (TA82)
Atopic eczema in under 12s: diagnosis and management (CG57)
Secondary bacterial infection of eczema and other common skin conditions: antimicrobial prescribing (NG190)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 29 studies.
Reviews & meta-analyses: 7 · Randomised trials: 2 · 2016–2025
Showing all 29 studies, sorted by most relevant.
N. Devasenapathy, A. Chu, M. Wong, et al.
The Lancet. Child & adolescent health, 2022
- Asthma
- Dermatitis, Atopic
- Hypersensitivity
T. Luger, Chia-Yu Chu, A. Elgendy, et al.
European Journal of Dermatology, 2023
Odeh Alsmeirat, S. Lakhani, Musab Egaimi, et al.
Cureus, 2022
Facial seborrheic dermatitis (SD) is a chronic inflammatory skin condition that can affect the quality of life with frequent recurrences. There is no medication as yet to cure this disease completely. There are four general categories of agents that are used to treat SD: antifungal agents, keratolytics, corticosteroids, and lastly calcineurin inhibitors. Topical therapies are the mainstream line of treatment to be used for this skin condition. The objective of this article is to critically review the published data in the literature on the use of topical pimecrolimus 1% topical cream as an option for treating facial SD. The final purpose of this review is to answer two questions: whether pimecrolimus topical cream is effective for the treatment of SD compared to the conventional current treatments and how safe is this treatment. The PubMed, Clinicaltrials.gov, MEDLINE + Embase, and Cochrane library databases were searched for original randomized clinical trials (RCTs) evaluating pimecrolimus 1% topical cream and comparing it with other topical treatments for SD. A systematic review and meta-analysis were then conducted on the selected studies by grading the evidence and qualitative comparison of results among and within studies. A total of five studies were included in the review; however, only four were eligible for inclusion in the meta-analysis, in which pimecrolimus was compared with other treatments for the management of facial SD. Pimecrolimus was found to be an effective topical treatment for facial SD, as it showed considerable desirable control of the symptoms in patients with facial SD clinically, in addition to a lower recurrence or relapsing rates; however, it had more side effects compared to other topical treatments, but the side effects were mild and tolerable.
Abstract licence: CC BY
Lixia Lai, Yanmei Wang, Luping Wen, et al.
Frontiers in Pharmacology, 2025
Background: Fumigation and sitz-bath therapy are traditional Chinese medicine (TCM) practices that offer unique benefits for managing chronic perianal eczema (CPE). This study aimed to investigate the clinical efficacy of the traditional Chinese herbal lotion (anal pruritus lotion, APL) combined with pimecrolimus cream in CPE treatment. Methods: Patients with CPE admitted between October 2019 and March 2022 were analyzed. The control group was given basic therapy with pimecrolimus cream, whereas the treatment group received pimecrolimus cream combined with APL under fumigation and sitz-bath therapy. We recorded and compared baseline patient information and clinical symptoms pre- and post-therapy, including clinical symptom scores, the eczema area and severity index (EASI), pruritus visual analogue scale (VAS) scores, dermatology life quality index (DLQI), and efficacy evaluations. Additionally, safety assessments and follow-up surveys were performed, as well. Results: < 0.05). Safety evaluations suggested that the treatments were safe and reliable. Conclusion: The combination of pimecrolimus cream and APL is more effective in the treatment of CPE than pimecrolimus cream alone, providing a promising new approach for the clinical management of perianal eczema. Clinical Trial registration: International Traditional Medicine Clinical Trial Registry, http://itmctr.ccebtcm.org.cn/en-US/Home/ProjectView?pid=58f1a168-bdf1-4e2a-a9bd-cf0f4a3ec06f as ITMCTR 2024000576.
Abstract licence: CC BY
O. M. Ezzatt, I. Helmy
Clinical Oral Investigations, 2018
- AC133 Antigen
- Administration, Topical
- Betamethasone
C. Chu, Tsung-Chieh Yao, I.-Hsin Shih, et al.
Dermatology and Therapy, 2023
Atopic dermatitis (AD) is a common chronic, multisystem inflammatory skin disease in pediatric patients. There has been an increase in the incidence of AD in the pediatric population of the Asia-Pacific region. Studies have shown that genetic, epigenetic, environmental and cultural factors may lead to differences in the clinical manifestation and prevalence of AD between races. Early treatment of AD is necessary to prevent the atopic march leading to comorbidities such as asthma and allergic rhinitis. Topical corticosteroids (TCS) are used as first-line therapy for the treatment of AD, but their long-term usage poses a risk to the patient's health. Pimecrolimus (1%) is a topical calcineurin inhibitor (TCI) that is indicated for the treatment of mild to moderate AD. Pimecrolimus has no apparent increase in adverse events compared to TCS, and it causes less of a burning sensation than tacrolimus. The safety and efficacy of pimecrolimus has been established through various clinical trials; yet, in many Asian countries, the use of pimecrolimus in infants is still restricted due to safety concerns. Based on the available evidence, the expert panel recommends pimecrolimus in infants between 3 months and 2 years of age in the Asian population.
Abstract licence: CC BY-NC
Ting Zhang, Fanzhang Meng, Junchen He, et al.
Frontiers in Allergy, 2025
Biologics targeting interleukin-17 (IL-17) are widely used for moderate to severe psoriasis with great efficiency. Nonetheless, their usage has sporadically resulted in paradoxical reactions, such as eczema, sarcoidosis-like eruptions, alopecia areata, and pyoderma gangrenosum. Here, we report a case of temporary facial eczema to secukinumab with a score of 5 on the Naranjo scale, which suggests a probable drug side effect. The patient was a 32-year-old Chinese male with a history of chronic plaque psoriasis for 5 years. He was previously treated with topical steroids, calcipotriol, narrowband ultraviolet B phototherapy, and oral traditional Chinese medicine intermittently since 2020. In January of 2025, his psoriasis exacerbated and was not well controlled. The patient underwent an initial regimen of 300 mg secukinumab once weekly for 4 weeks, with significant psoriasis area and severity index (PASI) improvement, and was scheduled to continue maintenance therapy on a regimen of every 4 weeks. However, in the seventh week of the secukinumab treatment course, the patient's face developed diffuse, swollen, erythematous patches that had almost coalesced into sheets. The surface is smooth, without scales, blisters, or exudation, and accompanied by mild itching. Lab tests show elevated alanine aminotransferase (ALT) at 83.2 U/L (normal range: 9-50 U/L), slightly increased direct bilirubin at 8.48 μmol/L (normal range: 0-8.0 μmol/L). Other lab tests showed no significant abnormalities. After oral compound glycyrrhizin, olopatadine hydrochloride, triprolidine hydrochloride, and topical pimecrolimus for a week, his facial lesions were completely cleared. Liver function tests normalized following a 2-week course of polyenphosphatidylcholine. The patient delayed secukinumab administration by 2 weeks and continued 300 mg secukinumab administration on a regimen of every 4 weeks. No recurrence of similar rash or other adverse effects was observed during the subsequent follow-up period over 5 months. It is concluded that eczema could be induced temporarily by secukinumab, and maybe continued application.
Abstract licence: CC BY
J. Castellsagué, J. Kuiper, A. Pottegård, et al.
Clinical Epidemiology, 2018
BACKGROUND: There is a concern that topical tacrolimus and pimecrolimus, indicated for second-line treatment of atopic dermatitis, may increase the risk of lymphoma and skin cancer, particularly in children. OBJECTIVE: The aim of this study was to compare incidence rates (IRs) of lymphoma and skin cancer between new users of topical tacrolimus or pimecrolimus and users of moderate- to high-potency topical corticosteroids (TCSs) and untreated subjects. METHODS: This is a multicenter cohort study with frequency matching by strata of propensity scores in population databases in the Netherlands, Denmark, Sweden, and the UK. IR ratios (IRRs) were estimated using Mantel-Haenszel methods for stratified analysis. RESULTS: We included 19,948 children and 66,127 adults initiating tacrolimus, 23,840 children and 37,417 adults initiating pimecrolimus, 584,121 users of TCSs, and 257,074 untreated subjects. IRs of lymphoma per 100,000 person-years were 10.4 events in children and 41.0 events in adults using tacrolimus and 3.0 events in children and 27.0 events in adults using pimecrolimus. The IRR (95% confidence interval [CI]) for lymphoma, tacrolimus versus TCSs, was 3.74 (1.00-14.06) in children and 1.27 (0.94-1.71) in adults. By lymphoma type, the highest IRR was 3.17 (0.58-17.23) for Hodgkin lymphoma in children and 1.76 (95% CI, 0.81-3.79) for cutaneous T-cell lymphoma (CTCL) in adults. For pimecrolimus versus TCSs, the highest IRR was 1.31 (95% CI, 0.33-5.14) for CTCL in adults. Compared with untreated subjects, adults using TCSs had a higher incidence of CTCL (IRR, 10.66; 95% CI, 2.60-43.75). Smaller associations were found between tacrolimus and pimecrolimus use and the risk of malignant melanoma or nonmelanoma skin cancer. CONCLUSION: Use of topical tacrolimus and pimecrolimus was associated with an increased risk of lymphoma. The low IRs imply that even if the increased risk is causal, it represents a small excess risk for individual patients. Residual confounding by severity of atopic dermatitis, increased monitoring of severe patients, and reverse causation could have affected the results.
Abstract licence: CC BY-NC
T. Luger, M. Augustin, J. Lambert, et al.
Pediatric Allergy and Immunology, 2020
- Dermatitis, Atopic
- Tacrolimus
- Consensus
Atopic dermatitis (AD) is a common skin disease during infancy, which imposes a considerable burden on patients, their families, and the society, requiring effective treatment options that result in rapid and sustained symptom relief. Additionally, early treatment may prevent the development of atopic comorbidities by restoring the skin barrier. Currently, topical standard-of-care for AD in infants includes emollients and topical corticosteroids (TCS) to treat and reduce the risk of flares. However, only few have been approved for infants and long-term maintenance therapy with TCS is not indicated due to potential local and systemic side effects, including skin atrophy. Accordingly, the recently updated European guidelines for treatment of AD recommend topical calcineurin inhibitors (TCIs) for long-term use, treatment of sensitive skin areas, and for use in the pediatric population. Evidence on the use of TCIs for infants has almost been exclusively collected for pimecrolimus, with >4000 infants evaluated in clinical trials, consistently confirming that pimecrolimus is a safe and effective treatment for infants with AD. Nevertheless, its use is still restricted in most countries to children above the age of 2 years due to initial and mostly theoretical safety concerns. Based on a careful review of the available evidence of clinical trials, post-marketing surveillance, and epidemiological studies, an Expert Panel of European dermatologists and pediatric allergologists concluded that these safety concerns are no longer valid. Therefore, pimecrolimus offers a safe and effective alternative to TCS in infants aged 3 months and above, and labeling restrictions in this age group are no longer justified.
Abstract licence: CC BY-NC
M. Ladda, V. Sandhu, A. Ighani, et al.
Journal of Cutaneous Medicine and Surgery, 2019
- Administration, Topical
- Hand Dermatoses
- Psoriasis
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Pimecrolimus binds with high affinity to macrophilin-12 (FKBP-12) and inhibits t…
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Protein binding
74%
Metabolism
Elimination
80%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 312 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:12087098 PMID:12150925 PMID:12150926 PMID:12231510 PMID:12718876 PMID:14651849 PMID:15268862 PMID:15467718 PMID:15545625 PMID:15718470 PMID:18497260 PMID:18762023 PMID:18925875 PMID:20516213 PMID:20537536 PMID:21659604 PMID:23429703 PMID:23429704 PMID:25799227 PMID:26018084 PMID:29150432 PMID:29236692 PMID:31112131 PMID:31601708 PMID:32561715 PMID:34519269 PMID:37751742
MTOR directly or indirectly regulates the phosphorylation of at least 800 proteins .
PMID:15268862 PMID:15467718 PMID:17517883 PMID:18372248 PMID:18497260 PMID:18925875 PMID:20516213 PMID:21576368 PMID:21659604 PMID:23429704 PMID:30171069 PMID:29236692 PMID:37751742
Functions as part of 2 structurally and functionally distinct signaling complexes mTORC1 and mTORC2 (mTOR complex 1 and 2) .
PMID:15268862 PMID:15467718 PMID:18497260 PMID:18925875 PMID:20516213 PMID:21576368 PMID:21659604 PMID:23429704 PMID:29424687 PMID:29567957 PMID:35926713
In response to nutrients, growth factors or amino acids, mTORC1 is recruited to the lysosome membrane and promotes protein, lipid and nucleotide synthesis by phosphorylating key regulators of mRNA translation and ribosome synthesis .
PMID:12087098 PMID:12150925 PMID:12150926 PMID:12231510 PMID:12718876 PMID:14651849 PMID:15268862 PMID:15467718 PMID:15545625 PMID:15718470 PMID:18497260 PMID:18762023 PMID:18925875 PMID:20516213 PMID:20537536 PMID:21659604 PMID:23429703 PMID:23429704 PMID:25799227 PMID:26018084 PMID:29150432 PMID:29236692 PMID:31112131 PMID:34519269
This includes phosphorylation of EIF4EBP1 and release of its inhibition toward the elongation initiation factor 4E (eiF4E) .
PMID:24403073 PMID:29236692
Moreover, phosphorylates and activates RPS6KB1 and RPS6KB2 that promote protein synthesis by modulating the activity of their downstream targets including ribosomal protein S6, eukaryotic translation initiation factor EIF4B, and the inhibitor of translation initiation PDCD4 .
PMID:12087098 PMID:12150925 PMID:18925875 PMID:29150432 PMID:29236692
Stimulates the pyrimidine biosynthesis pathway, both by acute regulation through RPS6KB1-mediated phosphorylation of the biosynthetic enzyme CAD, and delayed regulation, through transcriptional enhancement of the pentose phosphate pathway which produces 5-phosphoribosyl-1-pyrophosphate (PRPP), an allosteric activator of CAD at a later step in synthesis, this function is dependent on the mTORC1 complex .
PMID:23429703 PMID:23429704
Regulates ribosome synthesis by activating RNA polymerase III-dependent transcription through phosphorylation and inhibition of MAF1 an RNA polymerase III-repressor .
PMID:20516213
Activates dormant ribosomes by mediating phosphorylation of SERBP1, leading to SERBP1 inactivation and reactivation of translation .
PMID:36691768
In parallel to protein synthesis, also regulates lipid synthesis through SREBF1/SREBP1 and LPIN1 .
PMID:23426360
To maintain energy homeostasis mTORC1 may also regulate mitochondrial biogenesis through regulation of PPARGC1A (By similarity). In the same time, mTORC1 inhibits catabolic pathways: negatively regulates autophagy through phosphorylation of ULK1 .
PMID:32561715
Under nutrient sufficiency, phosphorylates ULK1 at 'Ser-758', disrupting the interaction with AMPK and preventing activation of ULK1 .
PMID:32561715
Also prevents autophagy through phosphorylation of the autophagy inhibitor DAP .
PMID:20537536
Also prevents autophagy by phosphorylating RUBCNL/Pacer under nutrient-rich conditions .
PMID:30704899
Prevents autophagy by mediating phosphorylation of AMBRA1, thereby inhibiting AMBRA1 ability to mediate ubiquitination of ULK1 and interaction between AMBRA1 and PPP2CA .
PMID:23524951 PMID:25438055
mTORC1 exerts a feedback control on upstream growth factor signaling that includes phosphorylation and activation of GRB10 a INSR-dependent signaling suppressor .
PMID:21659604
Among other potential targets mTORC1 may phosphorylate CLIP1 and regulate microtubules .
PMID:12231510
The mTORC1 complex is inhibited in response to starvation and amino acid depletion .
PMID:12150925 PMID:12150926 PMID:24403073 PMID:31695197
The non-canonical mTORC1 complex, which acts independently of RHEB, specifically mediates phosphorylation of MiT/TFE factors MITF, TFEB and TFE3 in the presence of nutrients, promoting their cytosolic retention and inactivation .
PMID:22343943 PMID:22576015 PMID:22692423 PMID:24448649 PMID:32612235 PMID:36608670 PMID:36697823
Upon starvation or lysosomal stress, inhibition of mTORC1 induces dephosphorylation and nuclear translocation of TFEB and TFE3, promoting their transcription factor activity .
PMID:22343943 PMID:22576015 PMID:22692423 PMID:24448649 PMID:32612235 PMID:36608670
The mTORC1 complex regulates pyroptosis in macrophages by promoting GSDMD oligomerization .
PMID:34289345
MTOR phosphorylates RPTOR which in turn inhibits mTORC1 (By similarity). As part of the mTORC2 complex, MTOR transduces signals from growth factors to pathways involved in proliferation, cytoskeletal organization, lipogenesis and anabolic output .
PMID:15268862 PMID:15467718 PMID:24670654 PMID:29424687 PMID:29567957 PMID:35926713
In response to growth factors, mTORC2 phosphorylates and activates AGC protein kinase family members, including AKT (AKT1, AKT2 and AKT3), PKC (PRKCA, PRKCB and PRKCE) and SGK1 .
PMID:15268862 PMID:15467718 PMID:21376236 PMID:24670654 PMID:29424687 PMID:29567957 PMID:35926713
In contrast to mTORC1, mTORC2 is nutrient-insensitive .
PMID:15467718
mTORC2 plays a critical role in AKT1 activation by mediating phosphorylation of different sites depending on the context, such as 'Thr-450', 'Ser-473', 'Ser-477' or 'Thr-479', facilitating the phosphorylation of the activation loop of AKT1 on 'Thr-308' by PDPK1/PDK1 which is a prerequisite for full activation .
PMID:15718470 PMID:21376236 PMID:24670654 PMID:29424687 PMID:29567957
mTORC2 also regulates the phosphorylation of SGK1 at 'Ser-422' .
PMID:18925875
mTORC2 may regulate the actin cytoskeleton, through phosphorylation of PRKCA, PXN and activation of the Rho-type guanine nucleotide exchange factors RHOA and RAC1A or RAC1B .
PMID:15268862
The mTORC2 complex also phosphorylates various proteins involved in insulin signaling, such as FBXW8 and IGF2BP1 (By similarity).
May also regulate insulin signaling by acting as a tyrosine protein kinase that catalyzes phosphorylation of IGF1R and INSR; additional evidence are however required to confirm this result in vivo .
PMID:26584640
Regulates osteoclastogenesis by adjusting the expression of CEBPB isoforms (By similarity). Plays an important regulatory role in the circadian clock function; regulates period length and rhythm amplitude of the suprachiasmatic nucleus (SCN) and liver clocks (By similarity)
PMID:15671020 PMID:18838687 PMID:19154138 PMID:23468591 PMID:30254215
Many of the substrates contain a PxIxIT motif and/or a LxVP motif .
PMID:17498738 PMID:17502104 PMID:22343722 PMID:23468591 PMID:27974827
In response to increased Ca(2+) levels, dephosphorylates and activates phosphatase SSH1 which results in cofilin dephosphorylation .
PMID:15671020
In response to increased Ca(2+) levels following mitochondrial depolarization, dephosphorylates DNM1L inducing DNM1L translocation to the mitochondrion .
PMID:18838687
Positively regulates the CACNA1B/CAV2.2-mediated Ca(2+) release probability at hippocampal neuronal soma and synaptic terminals (By similarity). Dephosphorylates heat shock protein HSPB1 (By similarity). Dephosphorylates and activates transcription factor NFATC1 .
PMID:19154138
In response to increased Ca(2+) levels, regulates NFAT-mediated transcription probably by dephosphorylating NFAT and promoting its nuclear translocation .
PMID:26248042
Dephosphorylates and inactivates transcription factor ELK1 .
PMID:19154138
Dephosphorylates DARPP32 .
PMID:19154138
May dephosphorylate CRTC2 at 'Ser-171' resulting in CRTC2 dissociation from 14-3-3 proteins .
PMID:30611118
Dephosphorylates transcription factor TFEB at 'Ser-211' following Coxsackievirus B3 infection, promoting nuclear translocation .
PMID:33691586
Required for postnatal development of the nephrogenic zone and superficial glomeruli in the kidneys, cell cycle homeostasis in the nephrogenic zone, and ultimately normal kidney function (By similarity).
Plays a role in intracellular AQP2 processing and localization to the apical membrane in the kidney, may thereby be required for efficient kidney filtration (By similarity). Required for secretion of salivary enzymes amylase, peroxidase, lysozyme and sialic acid via formation of secretory vesicles in the submandibular glands (By similarity). Required for calcineurin activity and homosynaptic depotentiation in the hippocampus (By similarity).
Required for normal differentiation and survival of keratinocytes and therefore required for epidermis superstructure formation (By similarity). Positively regulates osteoblastic bone formation, via promotion of osteoblast differentiation (By similarity). Positively regulates osteoclast differentiation, potentially via NFATC1 signaling (By similarity).
May play a role in skeletal muscle fiber type specification, potentially via NFATC1 signaling (By similarity). Negatively regulates MAP3K14/NIK signaling via inhibition of nuclear translocation of the transcription factors RELA and RELB (By similarity). Required for antigen-specific T-cell proliferation response (By similarity).
Dephosphorylates KLHL3, promoting the interaction between KLHL3 and WNK4 and subsequent degradation of WNK4 .
PMID:30718414
Negatively regulates SLC9A1 activity PMID:31375679
PPIases accelerate the folding of proteins. It catalyzes the cis-trans isomerization of proline imidic peptide bonds in oligopeptides
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC D11AH02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Pimecrolimus
Additional database identifiers
Drugs Product Database (DPD)
12077
ChemSpider
21111755
BindingDB
50248356
ZINC
ZINC000085536990
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3942
GenAtlas
FRAP1
GeneCards
MTOR
GenBank Gene Database
L34075
Guide to Pharmacology
2109
UniProt Accession
MTOR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9314
GeneCards
PPP3CA
GenBank Gene Database
L14778
GenBank Protein Database
306477
UniProt Accession
PP2BA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3711
GenAtlas
FKBP1A
GeneCards
FKBP1A
GenBank Gene Database
M34539
GenBank Protein Database
182628
Guide to Pharmacology
2609
UniProt Accession
FKB1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q417489), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.