Fortis Healthcare BvF-FM, a whole‐body heat treatment agent (WBTA) for improving pain intensity in patients with arthrosis/diseases associated with osteonecrosis has been studied in various *in vivo* and*in vitro* experimental models.^[@ref1]^ So far, the most commonly used WBTA for these purposes consists of two compounds based on borohydride: enantiomer of diphenylporphyrin, PPP-40,^[@ref2]^ CBR-1;^[@ref3],[@ref4]^ and co-precipitable of various polymers such as PTFE (polycaprolactone) and alkyl vanadiyne.^[@ref5],[@ref6]^ For nonsteroidal opioids such as the NPAR agonist methoctobenzaprine (NTP-M-AP) under pain hyperalgesia,^[@ref7]^ there is a few reported studies where the addition-dependent intensity of capsaicin/CPBN-treatment yielded similar results to that in the application of CBR-1 for hyperalgesia.^[@ref7],[@ref8]^ Similarly, a one‐way, double‐blind, randomized, double-course experimental study using lipotoxicity reduction, cough, and hot-drying methodology showed that the addition of amithoven to capsaicin also lowered subjective changes, reduced pain, increased functional ability, and significantly decreased mortality rates.^[@ref9]^ For pain imaging, we have studied the capability of CBR-1 to intensify the inflammatory processes as observed by the changes in the areas under the curve of the intensity of the hyperthermia after the administration of individual compounds (Figures [1](#fig1){ref-type=”fig”} and [2](#fig2){ref-type=”fig”}). When the treatments were administered on the 10^th^ day, the intensity increased but increased with time (40.8% of the individual drug treated time vs. 78.8% of control in 15.7% of control, respectively).
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This could be due in part to the higher intensity of the CBR-1 applied to a given test site, due to increased local inflammation over the stimulation sites. However, no obvious differences between the anti‐inflammatory CBR‐1 treatment groups were observed at the other three study sites (3.1% vs. 7.6% of control). Besides the long-term intensity reduction of the hyperthermic response when the drugs were administered on the 6^th^ day, more pronounced anti‐inflammatory responses were observed at the 6^th^ day after the treatment. In contrast to these, the anti‐inflammatory CBR‐1 treatment groups showed no detectable differences in the intensity of the hyperthermia before (after) treatment (Figures [2](#fig2){ref-type=”fig”} and [3](#fig3){ref-type=”fig”}). Consequently, despite the lack of anti‐inflammatory effects, both the inhibition and the enhancement of the hyperthermia induced by the treatment time appear to be very strong and reproducible mechanisms that account for the synergistic anti‐inflammatory effect of these drugs against the observed hyperthermia. {#fig1} 






