Hi again, I continued searching for studies regarding antihistamines and aPC and I e-mailed a professor Håkan Olsson from Lund University who has done previous studies on antihistamines and breast cancer. I asked him how the research field looks for advanced prostate cancer. This was his reply:
In Swedish:
”Vi har hittat 9 cancerformer varav prostatacancer är en av dem som har en förbättrad prognos efter desloratadinbruk. Jag har en doktorand som den11/9 presenterar dessa data i Lund vid sin disputation.
MVH
Håkan Olsson”
My translation (perhaps Google translate is better so I’ll post both)
”We have found 9 forms of cancer including prostate cancer that have a better prognosis after use of desloratadin. I have a postgraduade presenting these data on their dissertion 11/9 in Lund.”
I don’t know what to make of it yet but I found it intruguing! Also wonderful that you can simply e-mail a professor and get a reply on a Saturday night.
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TheTopBanana
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Thanks. So there is potential positive effect making the researchers more interested in these antihistamines. I also read a few articles about them on pubmed.
I needed a antihistamine earlier this year & began taking Claritin [Loratadine] before bed. I still do. Desloratadine is an active metabolite of Loratadine.
Olsson was in Texas in December, at the 2019 San Antonio Breast Cancer Symposium [1].
"We found a consistently beneficial effect of desloratadine use (HR = 0·67 ...) on survival, as well as of loratadine use (HR = 0·80 ...), regardless of age or estrogen receptor status, or whether breast cancer-specific or overall survival was analyzed, and a consistently negative effect on survival of clemastine use (HR = 1·45 ...).
"... We suggest immediate trials of desloratadine and loratadine as adjuvant treatment of breast cancer. Especially promising is the results for ER-breast cancer."
Abstract 5582: H1-antihistamines desloratadine and loratadine show potential for cancer therapy
Ildiko Fritz, Philippe Wagner and Hakan L. Olsson
DOI: 10.1158/1538-7445.AM2020-5582 Published August 2020
ArticleInfo & Metrics
Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA
Abstract
Antihistamines targeting histamine receptor H1make excellent candidates for drug repurposing for cancer therapy: they are safe drugs with minimal side effects that are well tolerated by most people, and evidence that they may be effective against tumors is mounting. Different mechanisms have been proposed for this potential effect: most are thought to be either wholly or partly histamine receptor H1independent, either involving lysosomal cell death or immunological pathways. We have previously found that use of certain H1-antihistamines is associated with substantially improved survival in both breast cancer1and cutaneous malignant melanoma (submitted), and here, we show that a similar association can be seen across multiple tumor types. Linking the cancer register, Drug Prescription Register and Cause of Death Register we have investigated use of the six most common H1-antihistamines used among Swedish cancer patients and survival in 16 different tumor types (n= 602 000), divided into two groups based on whether they have any known response to treatment with anti-immune checkpoint inhibition, such as anti-CTLA-4 or anti-PD-1 (immunogenic vs non-immunogenic tumors). The immunogenic group included cancer of the stomach, colon, rectum or anus, pancreas, lung, breast, prostate, kidney, bladder; and melanoma and Hodgkin lymphoma. The non-immunogenic group included tumors in the uterus, ovaries, brain and CNS, thyroid, liver and biliary tract and non-Hodgkin lymphoma. We choose to study the time period 2005-2014 because immune check point therapy was not yet used and antihistamines still were under patent protection and no off counter prescription occurred.We found that desloratadine use was associated with an improved survival for all the immunogenic tumors, including pancreatic cancer, but none of the non-immunogenic ones. Loratadine use was also associated with improved survival for some of the immunogenic tumors. The other antihistamines studied were consistently not associated with improved survival.Our hypothesis is that our findings have to do with immune checkpoint inhibition, though histamine receptor H1 inhibition as well as lysosomal cell death also may be involved.We believe that there is already a compelling case for initiation of clinical trials of certain H1-antihistamines, foremost among them desloratadine and loratadine, as treatment of both breast cancer and cutaneous malignant melanoma. Based on what we present here, that pool should be extended to include all other immunogenic tumors in our study and priority should be given to trials of desloratadine as treatment of pancreatic cancer, as the prognosis is dismal with highly limited treatment options available, and incidence is increasing. .1. Olsson HL, Einefors R, Broberg P. Second generation antihistamines after breast cancer diagnosis to improve prognosis both in patients with ER+ and ER- breast cancer. Journal of Clinical Oncology. 2015;33(15_suppl):3062-3062.
Citation Format: Ildiko Fritz, Philippe Wagner, Hakan L. Olsson. H1-antihistamines desloratadine and loratadine show potential for cancer therapy [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5582.
Possible Upside for people with CRPC can be great....otherwise what is the harm taking this safe anti histamine drug ? This goes into my "what is the harm" category along with sertraline, atorvastatin, Metformin, Doxycycline, losartan, cimetidine and others. To be kept an eye on future research about this "whats the harm" category.
Yes, the checkpoint inhibitor Ipilimumab is a lackluster therapy in PCa.
You might have been thinking of PARP inhibitors with respect to BRCA?
"The PARP inhibitors olaparib and rucaparib are now FDA approved for mCRPC patients with HRR mutations and BRCA1/2 mutations, respectively." [1] (8/17/20)
I'm not sure that the subset of men who might benefit from Ipilimumab has been well-defined yet.
"Since 2009, there have been 5 trials in mCRPC with ipilimumab (Table 3). A phase I/II study of patients receiving ipilimumab (10 mg/kg) with external beam radiation therapy showed that chemotherapy naïve patients may have more PSA responses (6 responders out of 23 patients, 26%) compared to chemotherapy experienced patients (2 responders out of 27 patients, 7.4%) (19). Similarly, a phase III study randomized 799 patients with mCRPC previously treated with chemotherapy to either ipilimumab plus radiation vs. placebo plus radiation. Although the primary endpoint of improved OS in the ipilimumab treated patients was not met, the ipilimumab arm had a superior progression free survival (PFS) (4.0 vs. 3.1 months) (11). A post-hoc analysis suggested a benefit with ipilimumab in patients with more favorable prognostic factors, specifically alkaline phosphatase ≤1.5 times the upper limit of normal, hemoglobin 11 g/dL and the absence of visceral metastases (11). In a second phase III study, using chemotherapy naïve patients who were either asymptomatic or minimally symptomatic, those with visceral metastases were excluded. This study randomized 602 patients to receive ipilimumab 10 mg/kg every 3 weeks for four doses or placebo. No difference in OS was observed, but patients treated with ipilimumab had a longer PFS (5.6 vs. 3.8 months, 95% CI, 0.55–0.81, HR 0.67) and were more likely to have a PSA response (23 vs. 8%) (12). Additionally, there is a study with finite ADT with ipilimumab in men with metastatic castration sensitive disease; 27 patients received 8 months of ADT with ipilimumab before the early termination of the study due to grade 3 irAEs in more than 40% of subjects (22). The 18 patients who did not progress during ADT had their ADT discontinued. The median time to PSA progression was 10.0 months following day 1 of ADT, and there were complete responses in 2 patients. The investigators found that clonal expansion of CD8+ T cells preceded the development of severe irAEs." [2] (8/7/20)
You are lucky to get a reply. Most can't be bothered. I email many researchers and academics. The response rate I guess is below 30%. Maybe they can't bring themselves to say 'dunno mate'...
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